In this case, when speaking of "reappearance of the symptoms when we lift the lower limb with the knee extended" we are describing the Lasègue Maneuver. This maneuver is positive in cases of lumbosciatic pain, since it causes a stretching of the sciatic nerve, therefore the correct answer is number 3. The rest of the pathologies do not have a positive Lasègue maneuver, so these options would not be correct.

In this case, when speaking of "reappearance of the symptoms when we lift the lower limb with the knee extended" we are describing the Lasègue Maneuver. This maneuver is positive in cases of lumbosciatic pain, since it causes a stretching of the sciatic nerve, therefore [HIDDEN]. The rest of the pathologies do not have a positive Lasègue maneuver, so these options would [HIDDEN].

A 61-year-old woman, administrative, with a history of overweight, hypertension, dyslipidemia and metabolic syndrome, who consults for pain in both buttocks, left trochanteric region, lateral aspect of the left thigh up to the knee and left leg up to the middle third. The pain appears when the lower limb is lifted with the knee extended, but is relieved when the knee is flexed. What is the first clinical suspicion?

Sacroiliac joint

Signs and symptoms The following are signs and symptoms that may be associated with an SI joint (SIJ) problem: Mechanical SIJ dysfunction usually causes a dull unilateral low back pain. The pain is often a mild to moderate ache around the dimple or posterior superior iliac spine (PSIS) region. The pain may become worse and sharp while doing activities such as standing up from a seated position or lifting the knee towards the chest during stair climbing. Pain is typically on one side or the other (unilateral PSIS pain), but the pain can occasionally be bilateral. When the pain of SIJ dysfunction is severe (which is infrequent), there can be referred pain into the hip, groin, and occasionally down the leg, but rarely does the pain radiate below the knee. Pain can be referred from the SIJ down into the buttock or back of the thigh, and rarely to the foot. Low back pain and stiffness, often unilateral, that often increases with prolonged sitting or prolonged walking.

Sciatica -- History and Physical

Further, a straight leg raise (SLR) test is a neurological maneuver performed while examining a patient presenting with lower back pain. This test is conducted with the patient lying supine while keeping the symptomatic leg straight by flexing the quadriceps. The examiner elevates the leg progressively at a slow pace. The test is deemed positive if it reproduces the patient's symptoms (pain and paresthesia) at an angle lower than 70° with radiation below the knee (Lasegue sign). This test is most helpful in diagnosing L4, L5, and S1 radiculopathies. The patient is asked to dorsiflex the foot while the examiner raises the leg (Bragaad sign) to increase the test's sensitivity. When executing the straight leg raise test, the examiner will slightly bend the patient's knee by 20° to 30°, which will lessen the pain. Then, manual pressure is applied in the popliteal fossa. The Bowstring sign is considered positive if it causes the same level of discomfort that the patient feels during a straight leg raise. [8] The Naffziger test involves reproducing pain via coughing. [9]

Sciatica -- History and Physical

A straight-leg raise has variable sensitivity and specificity and may or may not be present depending on the underlying cause. The straight-leg test is a passive examination where the patient first lies in a relaxed, supine position. The examiner then lifts the leg from the posterior aspect, flexing at the hip joint and keeping the knee in full extension or keeping the leg straight. Typically, pain that is reproduced between 30° to 70° of hip flexion and experienced primarily in the back is likely due to a lumbar disc herniation. Pain and parenthesis felt in the leg are possible due to lateralizing compression of a peripheral nerve. While not absolute, musculoskeletal causes of the pain usually reproduce pain above 70° of flexion and below 30° of flexion.

Greater trochanteric pain syndrome

More often the lateral hip pain is caused by disease of the gluteal tendons that secondarily inflames the bursa. This is most common in middle-aged women and is associated with a chronic and debilitating pain which does not respond to conservative treatment. Other causes of trochanteric bursitis include uneven leg length, iliotibial band syndrome, and weakness of the hip abductor muscles. Greater trochanteric pain syndrome can remain incorrectly diagnosed for years, because it shares the same pattern of pain with many other musculoskeletal conditions. Thus people with this condition may be labeled malingerers, or may undergo many ineffective treatments due to misdiagnosis. It may also coexist with low back pain, arthritis, and obesity. Signs and symptoms The primary symptom is hip pain, especially hip pain on the outer (lateral) side of the joint. This pain may appear when the affected person is walking or lying down on that side. Diagnosis

Lumbar Disc Herniation -- History and Physical

A straight leg raise test is a neurological maneuver performed while examining a patient presenting with lower back pain. It is conducted with the patient lying supine while keeping the symptomatic leg straight by flexing the quadriceps. The examiner slowly elevates the leg progressively at a slow pace. The test is positive when it reproduces the patient's symptoms (pain and paresthesia) at an angle lower than 45 degrees with radiation below the knee (Lasegue sign). It is most helpful in diagnosing L4, L5, and S1 radiculopathies. The patient is asked to dorsiflex the foot while the examiner is raising the leg (Bragaad's sign) to increase the sensitivity of the test.

[Diagnosis and treatment of lumbar spinal canal stenosis].

Lumbar spinal canal stenosis (LSCS) was first described in 1954 by Verbiest, followed by the currently accepted international classification of LSCS in 1976 by Arnoldi. Briefly, LSCS is a nervous system syndrome that is characterized by neural symptoms in the lower extremities due to tightened cauda equina and spinal nerve root involvement. LSCS international classification consists of: (1) degenerative, (2) congenital developmental, (3) combined, (4) spondylolytic spondylolisthesis, (5) iatrogenic and (6) post traumatic stenosis. Degenerative stenosis-the most common type of LSCS-is caused by disc degeneration, osteoarthritis of the facet joint and hypertrophy of the ligamentum flavum. LSCS may also be the result of intervertebral disc degeneration, protruded intervertebral disc and/or bony spur compress cauda equina and spinal nerve root anteriorally, while degenerated facet joint and hypertrophied the ligamentum flavum compress cauda equina and spinal nerve root posteriorally? Most often, spondylolytic spondylolisthesis occurs at the fourth lumbar vertebrae in middle-aged women. As a result of a slipping forward of the vertebra, cauda equina and spinal nerve roots can be tightened between the edge behind the top of lower vertebra and frontal edge of the lower part of upper lamina. Typical clinical symptoms of LSCS are low back pain, leg pain and intermittent claudication. Low back pain is chronic with secondary radiating pain in the buttock. The leg pain is called "sciatica", which tends to appear on the back of thigh, in the lateral aspect of lower leg and calf muscles, and which intensifies when the patient is fatigued. Intermittent claudication is a symptom associated with this syndrome. Often, patients with LSCS find it impossible to walk because of increased numbness and pain in their leg. Many patients report that after squatting for a few minutes they are able to resume walking. LSCS patients may also report dysaesthesia in the perineum area, and may also report urinary dysfunction ranging from extreme urgency to urinary delay. Patients who present with symptoms of LSCS should be seen by an orthopedic surgeon. Correct diagnosis by imaging and clinical examination, with appropriate conservative or operative treatment in a timely fashion should be encouraged in order to prevent irreversible nerve damage.

Disc Herniation -- History and Physical -- Physical Examination

L5 Nerve - back, radiating into buttock, lateral thigh, lateral calf, and dorsum foot, great toe; sensory loss on the lateral calf, dorsum of the foot, webspace between first and second toe; weakness on hip abduction, knee flexion, foot dorsiflexion, toe extension and flexion, foot inversion and eversion; decreased semitendinosus/semimembranosus reflex. S1 Nerve - back, radiating into buttock, lateral or posterior thigh, posterior calf, lateral or plantar foot; sensory loss on the posterior calf, lateral or plantar aspect of foot;  weakness on hip extension, knee flexion, plantar flexion of the foot; Achilles tendon; Medial buttock, perineal, and perianal region; weakness may be minimal, with urinary and fecal incontinence as well as sexual dysfunction. S2-S4 Nerves - sacral or buttock pain radiating into the posterior aspect of the leg or the perineum; sensory deficit on the medial buttock, perineal, and perianal region; absent bulbocavernosus, anal wink reflex.

Low back pain

Low back pain may be classified based on the signs and symptoms. Diffuse pain that does not change in response to particular movements, and is localized to the lower back without radiating beyond the buttocks, is classified as nonspecific, the most common classification. Pain that radiates down the leg below the knee, is located on one side (in the case of disc herniation), or is on both sides (in spinal stenosis), and changes in severity in response to certain positions or maneuvers is radicular, making up 7% of cases. Pain that is accompanied by red flags such as trauma, fever, a history of cancer or significant muscle weakness may indicate a more serious underlying problem and is classified as needing urgent or specialized attention.

Lumbosacral Facet Syndrome -- History and Physical

In most presentations, facetogenic lumbosacral pain often presents secondary to chronic pain alone. It should, however, be noted that facet joint pain may be referred distally into the lower limb, thus mimicking sciatica. In these cases of "pseudo-radicular" lumbar pain, patients typically experience radiation into the unilateral or bilateral buttocks and the trochanteric region (from L4 and L5 levels), the groin and thighs (from L2 to L5), ending above the knee, and without any neurologic deficits. At times, pain may radiate further down the lower extremity reaching the foot, thus mimicking sciatic pain. This may occur especially in the setting of rather large synovial cysts causing direct mechanical compression and creating ensuing inflammation to further irritate the surrounding nerve roots. [15] Facet joint pain is typically worse in the mornings and following periods of inactivity. Stress exercise, lumbar spinal extension or rotary motions, standing or sitting positions, and facet joint palpation may also elicit lumbar facetogenic pain. [2]

GALS screen

Now ask the patient to do the following noting any painful, restricted or asymmetrical movements: Test rotation of the thoracic and lumbar spine. Gently hold the patient's hips still and ask them to: "Turn your shoulders round as far as you can to the left, then do the same to the right." Test lateral flexion of the thoracic and lumbar spine: "Stand up straight and then slide the palm of your right hand down your thigh towards your knee, bending your shoulder down to the side." "Now do the same with your left hand down your left leg." "Bend your left ear down towards your left shoulder and then your right ear down towards your right shoulder" to test for pain free cervical spine lateral flexion. Now test for stiffness or pain flexing or extending the cervical spine: "bend your neck forwards to try to touch your chin against your chest." "bend your neck back to lift your chin."

Surgery_Schwartz

heavy-muscled athletesVenous claudicationEntire leg, but usually worse in thigh and groinTight, bursting painAfter walkingSubsides slowlyRelief speeded by elevationHistory of iliofemoral deep venous thrombosis, signs of venous congestion, edemaNerve root compression (e.g., herniated disk)Radiates down leg, usually posteriorlySharp lancinating painSoon, if not immediately after onsetNot quickly relieved (also often present at rest)Relief may be aided by adjusting back positionHistory of back problemsSymptomatic Baker’s cystBehind knee, down calfSwelling, soreness, tendernessWith exercisePresent at restNoneNot intermittentIntermittent claudication (hip, thigh, buttock)Hip, thigh, buttocksAching discomfort, weaknessAfter same degree of exerciseQuickly relievedNoneReproducibleHip arthritisHip, thigh, buttocksAching discomfortAfter variable degree of exerciseNot quickly relieved (and may be present at rest)More comfortable sitting, weight taken off legsVariable, may relate to activity

Radicular Back Pain -- History and Physical

L2, L3, and L4 lumbar radiculopathies are considered a group. This group has a marked overlap of the innervation of the anterior thigh muscles. [1] An acute injury in the distribution of L2, L3, and L4 will most commonly present with the patient experiencing radiating back pain to the anterior aspect of the thigh, which may progress into their knee, and possibly radiate to the medial aspect of the lower leg, into the foot. On examination, patients can have weakness during knee extension, hip adduction, and or hip flexion. There is often a loss of sensation over the anterior thigh along the area of pain. The patient may show a reduced patellar reflex (L4). [1] Activities that can make the symptoms worse include coughing, leg straightening, or sneezing.

Greater trochanteric pain syndrome: a review of anatomy, diagnosis and treatment.

Greater trochanteric pain syndrome (GTPS) is a term used to describe chronic pain overlying the lateral aspect of the hip. This regional pain syndrome, once described as trochanteric bursitis, often mimics pain generated from other sources, including, but not limited to myofascial pain, degenerative joint disease, and spinal pathology. The incidence of greater trochanteric pain is reported to be approximately 1.8 patients per 1000 per year with the prevalence being higher in women, and patients with coexisting low back pain, osteoarthritis, iliotibial band tenderness, and obesity. Symptoms of GTPS consist of persistent pain in the lateral hip radiating along the lateral aspect of the thigh to the knee and occasionally below the knee and/or buttock. Physical examination reveals point tenderness in the posterolateral area of the greater trochanter. Most cases of GTPS are self-limited with conservative measures, such as physical therapy, weight loss, nonsteroidal antiinflammatory drugs and behavior modification, providing resolution of symptoms. Other treatment modalities include bursa or lateral hip injections performed with corticosteroid and local anesthetic. More invasive surgical interventions have anecdotally been reported to provide pain relief when conservative treatment modalities fail.

InternalMed_Harrison

2692 LATERAL FEMORAL CUTANEOUS NEUROPATHY (MERALGIA PARESTHETICA) The lateral femoral cutaneous nerve arises from the upper lumbar plexus (spinal levels L2/3), crosses through the inguinal ligament near its attachment to the iliac bone, and supplies sensation to the anterior lateral thigh. The neuropathy affecting this nerve is also known as meralgia paresthetica. Symptoms and signs consist of paresthesias, numbness, and occasionally pain in the lateral thigh. Symptoms are increased by standing or walking and are relieved by sitting. There is normal strength, and knee reflexes are intact. The diagnosis is clinical, and further tests usually are not performed. EDx is only needed to rule out lumbar plexopathy, radiculopathy, or femoral neuropathy. If the symptoms and signs are classic, EMG is not necessary. Symptoms often resolve spontaneously over weeks or months, but the patient may be left with permanent numbness. Treatment consists of weight loss and avoiding tight belts. Analgesics

Spinal Stenosis -- History and Physical

Stenosis in the lumbar spine can lead to neurogenic claudication, myeloradiculopathy symptoms, sensory disturbances, motor weakness, and pathologic reflexes. Patients will present with complaints of cramping pain in the leg, calf, and or buttocks. They might report an increase in pain with walking or standing for prolonged periods and relief when sitting or leaning forward while using a shopping cart. [9] Disk herniation is most common at the L4-5 and L5-S1 levels. A herniated disk at L5-S1 can lead to plantarflexion weakness, decrease sensation in the lateral foot, and cause pain in the posterior leg. A disk herniation at L4-5 can lead to a foot drop and numbness in the large toe web and dorsal aspect of the foot. Lastly, an L3-4 disk herniation can lead to knee extension weakness, numbness in the medial foot, and pain in the anterior thigh.

Greater Trochanteric Pain Syndrome -- History and Physical

Patients with greater trochanteric pain syndrome usually have lateral hip pain, tenderness over and around the greater trochanter, pain at end-range hip rotation, abduction or adduction, pain with resisted hip abduction, and a positive Patrick-FABER (flexion abduction external rotation) test. Patients usually suffer from chronic back pain radiating to the posterolateral aspect of the thigh, leg paresthesias, and tenderness over the iliotibial tract. [6] They will often complain of the inability to lay on the affected hip. The mean duration of symptoms before treatment ranges from 7.1 weeks to 4.4 years. Young adults (18 to 35 years old) with hip pain often present with non-specific symptoms and vague findings from the history and physical examination, which may lead to a misdiagnosis of GTPS or trochanteric bursitis. [1] [4]

Neurology_Adams

The most characteristic syndrome affects the lumbar roots. Pain, which can be severe, begins in the low back or hip and spreads to the thigh and knee on one side; the discomfort has a deep, aching character with superimposed lancinating jabs and there is a propensity for pain to be most severe at night. Weakness and later atrophy are evident in the pelvic girdle and thigh muscles, although the distal muscles of the leg may also be affected. The weakness can progress for days or weeks (rarely, months). The patellar reflex is lost on the affected side. Curiously, we have found the opposite patellar reflex to be absent in some patients, without explanation. Deep and superficial sensation may be intact or mildly impaired, conforming to either a multiple nerve or multiple adjacent root distribution (i.e., L2 and L3, or L4 and L5). The pain lasts for several days and then gradually abates. Motor recovery is the rule although months and even years may elapse before it is complete. The same

Spinal gouty tophus presenting as an epidural mass lesion - A case report.

Gout is a metabolic disease secondary to an increased body pool of urate with hyperuricemia. Gout typically affects the peripheral joints and rarely involves the intra-spinal area. A 43-year-old man, who had metabolic syndrome s/p bariatric surgery and gout suffered from severe left low back pain with radiation to the lateral side of his left thigh and anterior side of his left leg for more than 7 days. His L-spine MRI showed an abnormal posterior epidural space occupying lesion at L4-L5 level. For tissue diagnosis and neural structures decompression, he underwent surgical removal of the epidural mass lesion. The surgical specimen showed a picture of gout and he got a good recovery after operation. The differential diagnoses of an epidural mass includes synovial cysts, ligament cyst, cystic neuromas, tumors, hematomas and abscesses. Gout in the spinal canal is difficult to diagnosis before surgery because it is rare and its clinical presentation and radiologic findings mimic tumor, abscess, tuberculosis, and degenerative spinal diseases. Patients with spinal gout may present with axial pain and a variety of neurological symptoms. Spinal gouty tophus should be considered in the different diagnoses of spinal epidural masses especially in patients with systemic gout. Surgery is needed for final diagnosis. If spinal gouty tophus is highly suspected during the surgery, the specimen should not be preserved with Formalin because birefringent crystals under polarized light is a unique feature for gouty tophus but they dissolve in Formalin.

A straight leg raising can be helpful in lumbosacral radiculopathy. The mechanism of pain during a straight leg raise is increased dural tension placed upon the lumbosacral spine during the test. Patients lay supine during the test. The physician will flex the patient's quadriceps with the leg in extension as well as dorsiflex the patient's foot on the symptomatic side. Pain or reproduction of paresthesias is considered a positive test (Lasegue's sign). A Bowstring sign relieves this underlying radicular pain with flexion of the patient's knee on the affected side. The straight leg raising test is most helpful in the diagnosis of L4 and S1 radiculopathies. [11] [3]

[Acromegaly and spinal canal stenosis].

A rare case of acromegaly with radiculomyelopathy due to spinal canal stenosis is reported. A long history of acromegalic deformity was seen on this 55 years old acupuncture therapist for the last 18 years, while he had developed unusually increased appetite, profuse perspiration and gained weight. Fifteen years ago, acromegalic tendency became prominent and was accompanied by low back and knee pain. In 1974 CB-154 was administered in several occasions beside 4000 rads irradiation to the sella. After radiation therapy was completed his outlook was somewhat improved, although low back pain was aggravated and associated with atrophy of the left lower extremity. The neurological examination at admission in 1980 revealed acromegalic feature, increased DTRs on both upper and lower extremities, dysesthesia of feet and atrophy of the leg muscles in general, mainly due to diffuse atrophy. Patient bended knees due to pain and unable to walk. He had radiating pain in the postero-lateral aspect of the left lower extremity and some dysesthesia of feet, although no specific root lesion was identifiable. Spinal roentgenograms disclosed diffuse ossification of anterior and posterior longitudinal ligaments, and marked spondylotic changes. Although the low back pain was impending complaint of the patient, the hypophyseal tumor was advised to remove and transsphenoidal hypophyseal adenomectomy was performed. A good amount of softend tumor tissue was removed however, adenoma found markedly fibrotic. Low back pain and knee were decreased gradually, but intermittent claudication was evident. Acromegaly in association with spinal canal stenosis were reviewed in literature, and the relationship of growth hormone and therapeutic problems were discussed.

Diabetic amyotrophy, not your typical back pain.

A 49-year-old man presented to the hospital for spinal cord decompression surgery with left buttock and left leg pain. The patient described an acute burning pain radiating down from his left buttock to left lateral leg. He also noted a 13.6 kg weight loss in recent months. Physical examination showed decreased muscle bulk of the left thigh, decreased strength of the left hip, left knee flexors and extensors. Recent MRI spine showed mild canal narrowing and cord flattening in the lower thoracic spine. Serologic testing showed an elevated glucose of 17.9 mmol/L and haemoglobin A1c of 9.8%. Electromyography showed denervation of scattered muscles of the left knee flexors, hip flexors and adductors. In the setting of newly diagnosed diabetes mellitus, he was diagnosed with diabetic amyotrophy, started on insulin therapy, and his surgery was cancelled.

Comparison of the history and physical examination for hip osteoarthritis and lumbar spinal stenosis.

Leg pain associated with walking is sometimes incorrectly attributed to hip osteoarthritis (OA) or lumbar spinal stenosis (LSS). This study compared physicians' values of signs and symptoms for diagnosing and differentiating hip OA and LSS to their clinical utility. Musculoskeletal physicians were surveyed with online questionnaires. Patients were recruited from hip and spine specialty practices. Seventy-seven hip OA and 79 LSS patients. Signs and symptoms of hip OA and LSS. Fifty-one of 66 invited musculoskeletal physicians completed online surveys about the values of 83 signs and symptoms for diagnosing hip OA and LSS. Of these, the most valued 32 symptoms and 13 physical examination items were applied to patients with symptomatic hip OA or LSS. Positive likelihood ratios (+LR) were calculated for each items' ability to differentiate hip OA from LSS, with a +LR>2 set as indicating usefulness for favoring either diagnosis. Positive LRs were compared with surveyed physicians' values for each test. All symptoms were reported by some patients with each diagnosis. Only 11 of 32 physician-valued symptoms were useful for discriminating hip OA from LSS. Eight symptoms favored hip OA over LSS: groin pain (+LR=4.9); knee pain (+LR=2.2); pain that decreased with continued walking (+LR=3.9); pain that occurs immediately with walking (+LR=2.4); pain that occurs immediately with standing (+LR=2.1); pain getting in/out of a car (+LR=3.3); pain with dressing the symptomatic leg (+LR=3.1); and difficulty reaching the foot of the symptomatic leg while dressing (+LR=2.3). Three symptoms favored LSS over hip OA: pain below the knee (+LR=2.3); leg tingling and/or numbness (+LR=2.7); and some pain in both legs (+LR=2.5). Notable symptoms that did not discriminate hip OA from LSS included: pain is less while pushing a shopping cart (+LR=1.0); back pain (+LR=1.1); weakness and/or heaviness of leg (+LR=1.1); buttocks pain (+LR=1.2); poor balance or unsteadiness (+LR=1.2); pain that increased with weight-bearing on the painful leg (+LR=1.3), and step to gait on stairs (+LR=1.7). Consistent with physicians' expectations, 7 of 13 physical examination items strongly favored hip OA over LSS: limited weight-bearing on painful leg when standing (+LR=10); observed limp (+LR=9); and painful and restricted range-of-motion with any of five hip maneuvers (+LR range 21-99). Four of five tested neurological deficits (+LR range 3-8) favored the diagnosis of LSS over hip OA. There is substantial crossover of symptoms between hip OA and LSS, with some physician-valued symptoms useful for differentiating these disorders whereas others were not. Physicians recognize the value of the examination of gait, the hip, and lower extremity neurological function for differentiating hip OA from LSS. These tests should be routinely performed on all patients for which either diagnosis is considered. Awareness of these findings might reduce diagnostic errors.

Pudendal tumor mimicking cauda equina syndrome and acute radiculopathy: case report.

Cauda equina syndrome (CES) is most caused by lumbar disc herniation, and the associated treatment involves prompt surgical decompression. Rarer causes of CES include perineural (Tarlov) cysts. A 62-year-old female with history of rheumatoid arthritis, hip and knee replacements, and chronic low back pain presented with worsening back pain, left leg weakness and pain for 6 weeks, and bowel/bladder incontinence with diminished sensation in the perianal region for 24 h prior to presentation. MRI demonstrated severe spinal stenosis at L4-S1, central disc herniation at L5-S1, and compression of the cauda equina, consistent with CES. A lumbar decompression was performed. Patient did well at 2-week follow up, but presented 5 weeks post-discharge with increased left leg pain/weakness and genitalia anesthesia. Imaging was unremarkable. Two months later, the patient presented with diminished sensation in the buttocks and bilateral lower extremities and bowel/bladder incontinence. Imaging demonstrated a large cystic presacral mass with involvement of the left sciatic foramen and S3 neural foramen. A team of plastic, orthopedic, and neurological surgeons performed an S3 sacral laminectomy, foraminotomy, partial sacrectomy, and S3 rhizotomy, and excision of the large left hemorrhagic pudendal mass. Final pathology demonstrated a perineural cyst with organizing hemorrhage. On follow-up, the patient's pain and weakness improved. CES-like symptoms were initially attributed to a herniated disk. However, lumbar decompression did not resolve symptoms, prompting further radiographic evaluation at two separate presentations. This represents the first reported case of a pudendal tumor causing symptoms initially attributed to a herniated disc.

Does this older adult with lower extremity pain have the clinical syndrome of lumbar spinal stenosis?

The clinical syndrome of lumbar spinal stenosis (LSS) is a common diagnosis in older adults presenting with lower extremity pain. To systematically review the accuracy of the clinical examination for the diagnosis of the clinical syndrome of LSS. MEDLINE, EMBASE, and CINAHL searches of articles published from January 1966 to September 2010. Studies were included if they contained adequate data on the accuracy of the history and physical examination for diagnosing the clinical syndrome of LSS, using a reference standard of expert opinion with radiographic or anatomic confirmation. Two authors independently reviewed each study to determine eligibility, extract data, and appraise levels of evidence. Four studies evaluating 741 patients were identified. Among patients with lower extremity pain, the likelihood of the clinical syndrome of LSS was increased for individuals older than 70 years (likelihood ratio [LR], 2.0; 95% confidence interval [CI], 1.6-2.5), and was decreased for those younger than 60 years (LR, 0.40; 95% CI, 0.29-0.57). The most useful symptoms for increasing the likelihood of the clinical syndrome of LSS were having no pain when seated (LR, 7.4; 95% CI, 1.9-30), improvement of symptoms when bending forward (LR, 6.4; 95% CI, 4.1-9.9), the presence of bilateral buttock or leg pain (LR, 6.3; 95% CI, 3.1-13), and neurogenic claudication (LR, 3.7; 95% CI, 2.9-4.8). Absence of neurogenic claudication (LR, 0.23; 95% CI, 0.17-0.31) decreased the likelihood of the diagnosis. A wide-based gait (LR, 13; 95% CI, 1.9-95) and abnormal Romberg test result (LR, 4.2; 95% CI, 1.4-13) increased the likelihood of the clinical syndrome of LSS. A score of 7 or higher on a diagnostic support tool including history and examination findings increased the likelihood of the clinical syndrome of LSS (LR, 3.3; 95% CI, 2.7-4.0), while a score lower than 7 made the diagnosis much less likely (LR, 0.10; 95% CI, 0.06-0.16). The diagnosis of the clinical syndrome of LSS requires the appropriate clinical picture and radiographic findings. Absence of pain when seated and improvement of symptoms when bending forward are the most useful individual findings. Combinations of findings are most useful for identifying patients who are unlikely to have the diagnosis.

Bilateral periprosthetic stress fractures in a juvenile chronic arthritis patient secondary to bilateral genu valgum.

Lateral insufficiency fractures following total hip replacement have been reported with the femoral stems positioned in varus, together with osteopenia of the lateral femoral cortex. Any abnormal alignment of the lower limbs, such as genu valgum, will alter the load distribution across the femoral cortices, and repetitive loading during walking will predispose the bones to stress fractures at any stress riser point, such as the tip of a femoral component. Bilateral femoral stress fractures post total hip replacements have not been previously described. We present a 55-year-old woman, diagnosed with juvenile idiopathic arthritis, who had undergone bilateral total hip replacements and bilateral knee replacements. The knees 15 years postoperatively were in valgus and the left knee was extremely stiff, flexing to just 5. The patient presented with bilateral thigh pain, with plain radiographs confirming bilateral periprosthetic fractures of the femur at the tip of well-fixed femoral components. There was no history of injury and her hips were functioning well up to this time. The patient required revision of both hips to long-stem uncemented components, bypassing the fractures, and revision of both knees to stemmed semi-constrained implants, thereby correcting the alignment of both lower limbs. Both fractures healed and the patient is currently pain-free and mobile with walking aids. Surgeons must remain aware that when implants are in situ, abnormal alignments will lead to abnormal forces, and stress fractures are likely to occur at any stress riser around the implant. Avoiding malalignment will avoid this complication.

Plantar Heel Pain -- History and Physical -- S1 Radiculopathy

Patients with heel pain may have a history of chronic lower back pain. Clinically, radicular involvement will present as pain and numbness radiating from the lower back down to the heel of the foot. Patients may have decreased sensation over the skin of the sole, heel, or lateral foot and weakness of the gastrocnemius, gluteus maximus, hamstring, peroneal, and foot muscles with a diminished ankle reflex. Perform the positive straight leg raise test (Lasègue test) with the patient in the supine position. Pain with passive hip flexion while lifting the leg suggests stretching the lower lumbar and sacral roots. [21] Perform a crossed straight leg raise test, eliciting pain on the contralateral side with the same motion. Results from new studies suggest that these exams may not be as reliable as we once thought. [22]

Neurogenic claudication

Knee to chest stretch - Laying down on the back, bring one leg up and pull it towards the chest and hold for 30–45 seconds. Posterior pelvic tilt (bridges) - Laying on the back, bend both legs and place your feet on the floor. Raise stomach from the ground, lifting the back and pelvis, until the back is straight. Hold for 5–10 seconds and relax. Neural Stretching of the legs - Laying on the back, bring one leg up with a stretching band until a stretch is felt in the legs. Ensure your legs are straight. Once the stretch is felt, hold for 30–45 seconds and relax. Hip-flexor stretch - To stretch the right hip-flexor, bring the left leg forward, and kneel on the right knee. Push the pelvis forward (lean forward), whilst keeping the upper body straight. Hold the position for 30–45 seconds and relax. To stretch the left hip-flexor, bring swap the positions of the legs.

Deep vein thrombosis in an athletic military cadet.

Resident's case problem. A 21-year-old healthy athletic male military cadet with complaint of worsening diffuse left knee pain was evaluated 4 days after onset. The knee pain began 2 hours after completing a long car trip, worsened over the subsequent 3 days, and became almost unbearable during the return trip. The patient reported constant pain, limited knee motion, and difficulty ambulating. In addition, he was unable to perform physical military training or attend academic classes due to the severe left knee pain. Past medical history revealed a mild left lateral calf strain 21/2 weeks prior, which completely resolved within 24 hours of onset. Our physical examination led us to either monoarticular arthritis, pseudothrombophlebitis (ruptured Baker's cyst), or a lower leg deep vein thrombosis (DVT) as the cause of knee pain. Diagnostic imaging of this patient revealed a left superficial femoral vein thrombosis and popliteal DVT, with bilateral pulmonary emboli (PE). A systematic differential diagnosis was undertaken to rule out a potentially fatal DVT diagnosis as the cause of knee pain, despite minimal DVT risk factors. The physical therapist in a direct-access setting must ensure timely evaluation and referral of a suspected DVT, even when patient demographics cause the practitioner to question the likelihood of this diagnosis. The physical examination findings, clinical suspicion, and established clinical prediction rules can accurately dictate the appropriate referral action necessary.

Multiple Venous Thromboses Presenting as Mechanical Low Back Pain in an 18-Year-Old Woman.

The purpose of this case report is to describe a patient who presented with acute musculoskeletal symptoms but was later diagnosed with multiple deep vein thrombosis (DVT). An 18-year-old female presented to a chiropractic clinic with left lumbosacral pain with referral into the posterior left thigh. A provisional diagnosis was made of acute myofascial syndrome of the left piriformis and gluteus medius muscles. The patient received 3 chiropractic treatments over 1 week resulting in 80% improvement in pain intensity. Two days later, a sudden onset of severe abdominal pain caused the patient to seek urgent medical attention. A diagnostic ultrasound of the abdomen and pelvis were performed and interpreted as normal. Following this, the patient reported increased pain in her left leg. Evaluation revealed edema of the left calf and decreased left lower limb sensation. A venous Doppler ultrasound was ordered. Doppler ultrasound revealed reduction of the venous flow in the femoral vein area. An additional ultrasonography evaluation revealed an extensive DVTs affecting the left femoral vein and iliac axis extending towards the vena cava. Upon follow-up with a hematologist, the potential diagnosis of May-Thurner syndrome was considered based on the absence of blood dyscrasias and sustained anatomical changes found in the left common iliac vein at its junction with the right common iliac artery. A week following discharge, she presented with chest pain and was diagnosed with venous thromboembolism. The patient was successfully treated with anticoagulation therapy and insertion of a vena cava filter. Although DVTs are common in the general population, presence in low-risk individuals may be overlooked. In the presence of subtle initial clinical signs such as those described in this case report, clinicians should keep a high index of suspicion for a DVT. Rapid identification of such clinical signs in association with a lack of objective examination findings warrants further evaluation due to potentially negative outcomes.

What was the disease of the legs that afflicted King Asa?

The elderly have suffered from pain in their legs, which may be associated with various diseases, for thousands of years. This report analyzes the disease that afflicted the biblical King Asa (the third king of the house of Judah who reigned between 867 and 906 BCE). The sentence 'Nevertheless in the time of his old age he was diseased in his legs' indicates that King Asa suffered from disease in his legs. Among numerous diseases, peripheral vascular disease, gout, and degenerative osteoarthritis were most likely to affect the King's legs. And among these diseases, the diagnosis of peripheral vascular disease is the most acceptable. This report shows that the roots of contemporary modern gerontology can be traced back to biblical times.

L5 nerve root exits at the L5-S1 foramina. When compressed by a herniated disc, it causes back pain that radiates into the buttock, lateral thigh, lateral calf, the dorsum of the foot, and the great toe. Sensory loss is present on the web space between the big toe and second toe, the dorsum of the foot, and lateral calf. There is a weakness in hip abduction, knee flexion, foot dorsiflexion, big toe dorsiflexion, foot inversion, and eversion. Patients present with decreased semitendinosus/semimembranosus reflex. Weakness in foot dorsiflexion makes it challenging to walk on the heels. Chronic L5 radiculopathy may cause atrophy of the extensor digitorum brevis and the tibialis anterior of the anterior leg.

Repetitive nerve block for neuropathic pain management: a case report.

Schwannoma is a common neoplasm in the peripheral and central nervous systems. Sciatic nerve schwanommas are rare. We report the case of a 50-year-old woman who was referred for treatment of persistent neuropathic pain in the left lower limb after resection of a schwannoma on the left S1 nerve root. The patient's history goes back when she was 27 years old and started to have electric-like pain in her lower left limb upon intercourse. Examination revealed a left ovarian cyst which was surgically removed. Her pain persisted despite taking nonsteroidal anti inflammatory drugs (NSAIDs). Several years later a schwannoma on the left S1 nerve root was detected. The patient had surgical excision of the left S1 nerve root at the plexus along with the schwannoma. Following the surgery, she experienced pain upon sitting and touch, and had a limp in her left leg. She was prescribed NSAIDs, antidepressant and pregabalin. Despite the pharmacological treatment, the patient had persistent mild pain. Upon physical examination, the incision from her previous surgery was 4 cm away from the sacral midline and parallel to S1 and S2. The length of the incision was 3 cm. The patient had severe allodynia upon palpation at the area between S1 and L5 and the visual analog scale (VAS) score increased from 3 to 10. She had severe pain at rest and movement. Her neurologic exam revealed that the left lower extremity motor power showed mild weakness in the leg abduction, foot eversion, plantar and toes flexion, and in the hip extension. The sensory exam showed severe reduction in pinprick and temperature sensation in the lateral aspect of foot, lower leg and dorsolateral thigh and buttocks. Nerve stimulator guided injection was performed at the pain trigger point being 1 cm above the midline of the incision. Upon nerve stimulation the contraction of the gluteal muscle was observed. Then, 20 mL of the anesthetic mixture were injected. The patient had immediate pain relief after the block (VAS 1/10). She remained pain free for 15 days after which pain reappeared but with less severity (3/10). Repetitive sciatic nerve block was performed in a progressive manner and was shown to be effective in managing neuropathic pain.


This year's Neurology section's burning question. He presents a diabetic patient on insulin treatment with good control (although diabetic neuropathies do not only develop in patients with poor control) with a sensory picture limited to the upper limbs and of short onset time, without motor symptoms or at any other level. In the examination there is a clear dissociation with thermoalgesic anesthesia and preservation of arthrokinetic and vibratory. Reflexes are normal, neither abolished nor exalted. In addition, the rest of the examination is strictly normal. With all this I believe that the correct answer is 5, that is a syringomyelic lesion, whose initial characteristic is the sensitive dissociation with anesthesia for the thermoalgesic and conservation of the posterior cord. MS and other spinal cord lesions would be accompanied by other exploratory signs such as exaltation of reflexes, for carpal tunnel the exploration exceeds the territory distal to the carpus, and as for answer 1, although there are forms of peripheral polyneuropathy "pseudosyringomyelic" they are usually of lumbar onset. The short evolution time (2 weeks), the respect of the lower limbs and the preservation of muscle reflexes make me rule out this response despite the distribution being "glove-like".

This year's Neurology section's burning question. He presents a diabetic patient on insulin treatment with good control (although diabetic neuropathies do not only develop in patients with poor control) with a sensory picture limited to the upper limbs and of short onset time, without motor symptoms or at any other level. In the examination there is a clear dissociation with thermoalgesic anesthesia and preservation of arthrokinetic and vibratory. Reflexes are normal, neither abolished nor exalted. In addition, the rest of the examination is strictly normal. With all this I believe that [HIDDEN], that is a syringomyelic lesion, whose initial characteristic is the sensitive dissociation with anesthesia for the thermoalgesic and conservation of the posterior cord. MS and other spinal cord lesions would be accompanied by other exploratory signs such as exaltation of reflexes, for carpal tunnel the exploration exceeds the territory distal to the carpus, and as for answer 1, although there are forms of peripheral polyneuropathy "pseudosyringomyelic" they are usually of lumbar onset. The short evolution time (2 weeks), the respect of the lower limbs and the preservation of muscle reflexes make me rule out this response despite the distribution being "glove-like".

A 32-year-old diabetic patient on insulin therapy with good control of his blood glucose levels comes to your office with tingling in both hands, with a sensation of corking and thermal insensitivity of progressive onset over the course of 2 weeks. She does not report visual disturbances, strength deficit, motor clumsiness or other symptoms. On examination she found anesthesia to pain and temperature in both hands and distal forearms; positional and vibratory sensitivity were preserved. There is no muscle atrophy or strength deficit. Muscle reflexes are normal and symmetrical. There is no dysmetria, dysdiadochokinesia or intention tremor. The rest of the neurological examination is strictly normal. Indicate the most likely diagnosis in this case:

Peripheral sensitvo symmetric distal peripheral neuropathy of diabetic cause.

Compressive cervical spinal cord injury.

Multiple sclerosis type demyelinating disease.

Intention tremor

Intention tremors can be a first sign of multiple sclerosis, since loss or deterioration of motor function and sensitivity are often one of the first symptoms of cerebellar lesions. Intention tremors have a variety of other recorded causes as well. These include a variety of neurological disorders, such as stroke, alcoholism, alcohol withdrawal, peripheral neuropathy, Wilson's disease, Creutzfeldt–Jakob disease, Guillain–Barré syndrome and fragile X syndrome, as well as brain tumors, low blood sugar, hyperthyroidism, hypoparathyroidism, insulinoma, normal aging, and traumatic brain injury. Holmes tremor, a rubral or midbrain tremor, is another form of tremor that includes intention tremors, among other symptoms. This disease affects the proximal muscles of the head, shoulders, and neck. Tremors of this disease occur at frequencies of 2–4 Hz or more.

[A Case of Hirayama Disease Presenting Horn Hand: Spinal Horn Hand].

A 28-year-old man with Hirayama disease presented with a peculiar hand posture called "horn hand" ("main en corne"). The patient noticed that he could not extend his 3rd and 4th fingers when extending the fingers of his right hand 1 year prior to presentation. On neurological examination, the strength of the finger extension is severely weak in the 1st, 3rd and 4th fingers, causing a drop finger posture, but it is only moderately weak in the 2nd and 5th fingers, enabling him to sustain the extension finger posture. The finger posture is like a bull's horns and is named "horn hand". Amyotrophy of the ulnar side of the right forearm, so-called "oblique amyotrophy", and amyotrophy of the right hand are observed. MRI examination reveals atrophy of the lower cervical spinal cord and compression of it in the neck flexion posture. Diagnosis of Hirayama disease (juvenile muscular atrophy of the distal upper extremity) is confirmed. Horn hand has been reported so far in some cases of lead neuropathy, chronic inflammatory demyelinating polyneuropathy, and distal myopathy; a "peripheral" horn hand is characterized by partial and selective lesion of the radial nerve or of the finger extensor muscles. Meanwhile, a "spinal" horn hand in this patient with Hirayama disease represents the partial and selective lesion of the spinal anterior horn neurons.

Amyotrophy

Amyotrophy is progressive wasting of muscle tissues. Muscle pain is also a symptom. It can occur in middle-aged males with type 2 diabetes. It also occurs with motor neuron disease. Differential diagnosis The following are considered differential diagnosis for Amyotrophy: compressive and infective causes of polyradiculopathy structural disc diseases chronic demyelinating neuropathies See also Diabetic amyotrophy Monomelic amyotrophy Amyotrophic lateral sclerosis References External links Muscular disorders

[An elderly case of juvenile muscular atrophy in the unilateral upper extremity with tremor in both hands].

A 75-year-old man had noticed muscle atrophy and weakness of his right hand and forearm at the age of 25. The symptoms slowly progressed and then stopped. Right hand tremor appeared at about age 40. There was no symptom in his left upper extremity, and his gait was normal. He now shows severe muscle atrophy in his right hand and forearm. There was distally dominant weakness of the right upper extremity and his hand grip was 0 kg on the right and 25 kg on the left. On admission there was no weakness in the bilateral lower extremities. He had postural tremor in both hands and fingers. The tendon reflexes were hypoactive in the upper extremities and normal in the lower extremities. Abnormalities in the superficial sensation were unremarkable, whereas vibration sensation in both the upper and lower extremities was mildly disturbed. Electromyography revealed chronic denervation, especially in the right upper extremity. The sensory nerve conduction study results and somatosensory evoked potentials in the upper extremities were normal. Cervical MRI demonstrated spondylotic changes, canal stenosis from the C5 to C7 levels, and compression of the spinal cord. His hand tremor was dominant on the right with a peak frequency of about 7 Hz. Tremor frequency and power were decreased by mechanical load. Hirayama's disease (juvenile muscular atrophy of unilateral upper extremity) was the most probable diagnosis, although aging might have produced various additional abnormalities. The tremor seen in this patient showed characteristics of enhanced physiological tremor.

Monomelic amyotrophy

The disease is rare and several cited cases deviate from the expected norm, making diagnosis more difficult. Proposed diagnostic criteria: Distal predominant muscle weakness and atrophy in forearm and hand Involvement of the unilateral upper extremity almost always all the time Onset between the ages of 10 to early 20s Insidious onset with gradual progression for the first several years, followed by stabilization No lower extremity involvement No sensory disturbance and tendon reflex abnormalities Exclusion of other diseases (e.g., motor neuron disease, multifocal motor neuropathy, brachial plexopathy, spinal cord tumors, syringomyelia, cervical vertebral abnormalities, anterior interosseous, or deep ulnar neuropathy)

Hand Nerve Compression Syndromes -- History and Physical -- Median Nerve

Median nerve compression at the hand and wrist is called carpal tunnel syndrome. It is the most common type of nerve injury and results from compression of the median nerve at the wrist as it passes between the carpal bones and the flexor retinaculum. It is typically the result of repetitive use of the hands but can be the result of other factors such as obesity, diabetes, pregnancy, and hypothyroidism. Patients often report numbness, tingling, and pain that worsens at night. These symptoms can be elicited from activities that involve prolonged wrist flexion and/or extension. Shaking the hand may alleviate the symptoms. They may also be weakness and clumsiness of the hand with activities such as gripping and grasping. The physical exam is an important component in the diagnosis of carpal tunnel as it can help distinguish carpal tunnel from other diagnoses such as proximal median neuropathy (pronator syndrome) and cervical radiculopathy. Sensory symptoms involve the thumb, index, long, and lateral half of the ring finger. There will be no sensory loss at the thenar eminence with carpal tunnel syndrome when compared to more proximal lesions. If motor weakness is present, it is typically evident with weakness of thumb abduction. There may also be atrophy of the thenar eminence as the median nerve innervates many muscles in this region. Signs that will be absent in carpal tunnel syndrome include weakness in forearm pronation, finger abduction, and finger extension. There are several provocative tests used to diagnose carpal tunnel syndrome [8] [10] :

Median Nerve Palsy -- History and Physical

Diagnosticians must always evaluate the neck in patients with presumed median nerve injury or carpal tunnel syndrome. Double crush syndrome is defined as an injury to a nerve at both a distal site of compression as well as proximally such as in the case of a coexistent cervical disk herniation or foraminal stenosis. This condition is most commonly identified when patients have an unsatisfactory resolution of symptoms after a carpal tunnel release. [10] Osterman et al. found in a prospective study that patients who suffered from double crush syndrome reported more "paresthesias" rather than "numbness" compared to patients who had isolated carpal tunnel syndrome. He also found that grip strength was decreased more with double crush syndrome compared to carpal tunnel syndrome. [11] Of note, radiography of the cervical spine is not currently recommended for evaluation of double crush syndrome by current literature, particularly in the older patient population as there is a very high incidence of asymptomatic degenerative changes of the spine. MRI may be useful but is cost-prohibitive and not necessary in most cases. Therefore, history and physical examination with documentation of such examination techniques as Spurling's cervical spine maneuver to identify cervical nerve root compression, are important tools to identify double crush syndromes. [10] [12] [13]

Peripheral neuropathy

Most types of polyneuropathy progress fairly slowly, over months or years, but rapidly progressive polyneuropathy also occurs. It is important to recognize that at one time it was thought that many of the cases of small fiber peripheral neuropathy with typical symptoms of tingling, pain, and loss of sensation in the feet and hands were due to glucose intolerance before a diagnosis of diabetes or pre-diabetes. However, in August 2015, the Mayo Clinic published a scientific study in the Journal of the Neurological Sciences showing "no significant increase in...symptoms...in the prediabetes group", and stated that "A search for alternate neuropathy causes is needed in patients with prediabetes." The treatment of polyneuropathies is aimed firstly at eliminating or controlling the cause, secondly at maintaining muscle strength and physical function, and thirdly at controlling symptoms such as neuropathic pain.

Monomelic amyotrophy

In early stages of the disease MMA may be confused for amyotrophic lateral sclerosis (ALS), cervical spondylotic amyotrophy (CSA), and other challenging neurological diseases, as well as conditions that are minor but that call for very different treatments, such as advanced carpal tunnel syndrome (CTS). Symptoms somewhat differ. Pain and tingling in the hand is typically present in CTS and absent from MMA; loss of function presents differently; with careful electrophysiological study and neurological exams the two are distinguished. In early stages, ALS, SCA, and MMA, presentation may be similar. Both CSA and ALS ultimately have more extensive symptoms. MMA is more prevalent in young people while ALS and CSA are more common in older populations. With ALS, hand symptoms usually more commonly both proximal and distal vs in MMA mostly distal only, and with ALS fasciculations (twitching) are often present in upper extremities, but rarely in MMA. MMA is usually eliminated from

Neurology_Adams

Over the years, the authors have encountered young men with localized and asymmetrical amyotrophy of the forearm that became arrested and did not advance over a decade or two, typical of Hirayama disease. Reports of such a partial cervical spinal amyotrophy have appeared (Hirayama et al; Moreno Martinez et al). In the type described by Hirayama and associates, young men are affected with progressive and asymmetrical amyotrophy of the forearm and hand that has been traced to ligamentous hypertrophy and buckling in the ventral spinal canal. This causes a compression of the cervical spinal cord gray matter, presumably by a chronic ischemic effect as discussed in detail in Chap. 42. In a familial variety of pure restricted amyotrophy, only the vocal cords became paralyzed over a period of years in adult life; only later were the hands affected.

Neurology_Adams

Unlike herniated lumbar discs, cervical ones, if large and centrally situated, result in compression of the spinal cord (Fig. 10-6). The centrally situated disc is often painless, and the cord syndrome may simulate multiple sclerosis or a degenerative neurologic disease. Bilateral hand numbness, paresthesia, or similar altered sensation is common. Failure to consider a protruded cervical disc in patients with obscure symptoms in the legs, including stiffness and falling, is a common error. A vague sensory change can often be detected on the thorax, the rostral margin of which is several dermatomes below the level of compression. The diagnosis and the level of disc protrusion can be confirmed by MRI or by CT myelography. Nerve conduction studies, F responses, and EMG are helpful in confirming the level of root compression and distinguishing pain of radicular origin from that originating in the brachial plexus or in individual nerves of the arm (see “Brachial Neuritis” in Chap. 43).

InternalMed_Harrison

Isolated mononeuropathies may cause symptoms beyond the territory supplied by the affected nerve, but abnormalities on examination typically are confined to appropriate anatomic boundaries. In multiple mononeuropathies, symptoms and signs occur in discrete territories supplied by different individual nerves and—as more nerves are affected—may simulate a polyneuropathy if deficits become confluent. With polyneuropathies, sensory deficits are generally graded, distal, and symmetric in distribution (Chap. 459). Dysesthesias, followed by numbness, begin in the toes and ascend symmetrically. When dysesthesias reach the knees, they usually also have appeared in the fingertips. The process is nerve length–dependent, and the deficit is often described as “stocking-glove” in type. Involvement of both hands and feet also occurs with lesions of the upper cervical cord or the brainstem, but an upper level of the sensory disturbance may then be found on the trunk and other evidence of a central

Hand injury

Carpal tunnel syndrome is a common disorder of the hand. This disorder results from compression of an important nerve in the wrist. Disorders like diabetes mellitus, thyroid or rheumatoid arthritis can narrow the tunnel and cause impingement of the nerve. Carpal tunnel syndrome also occurs in people who overuse their hand or perform repetitive actions like using a computer key board, a cashiers machine or a musical instrument. When the nerve is compressed, it can result in disabling symptoms like numbness, tingling, or pain in the middle three fingers. As the condition progresses, it can lead to muscle weakness and inability to hold objects. The pain frequently occurs at night and can even radiate to the shoulder. Even though the diagnosis is straightforward, the treatment is not satisfactory.

InternalMed_Harrison

both hands and feet also occurs with lesions of the upper cervical cord or the brainstem, but an upper level of the sensory disturbance may then be found on the trunk and other evidence of a central lesion may be present, such as sphincter involvement or signs of an upper motor neuron lesion (Chap. 30). Although most polyneuropathies are pansensory and affect all modalities of sensation, selective sensory dysfunction according to nerve fiber size may occur. Small-fiber polyneuropa-161 thies are characterized by burning, painful dysesthesias with reduced pinprick and thermal sensation but with sparing of proprioception, motor function, and deep tendon reflexes. Touch is involved variably; when it is spared, the sensory pattern is referred to as exhibiting sensory dissociation. Sensory dissociation may occur also with spinal cord lesions as well as small-fiber neuropathies. Large-fiber polyneuropathies are characterized by vibration and position sense deficits, imbalance, absent tendon

[Compressive ischemic neuropathies of the upper extremities and work].

The objective of the presented study was to motile that cumulative trauma disorders of the upper extremities in recent years leads to arising morbidity and applications for compensation for occupational diseases. This rise is probably not associated with an increase of this disorder but a different awareness of workers and doctors as regards the possible adverse effect of forceful and frequently repeated movements of the upper extremities on their function, extended diagnostics and notification. It is important to master the diagnosis of these diseases and interpretation of auxiliary examinations to prevent inadequate payment of damages to the affected subjects and on the other hand to prevent breakdown or in adequate function of the financial provisions in this area. A number of syndromes of the mentioned conditions has very few objective symptoms and abnormal results of auxiliary examinations. The diagnosis of stenotic syndromes has a compared with other disorders great support in electrophysiological techniques, their high sensitivity and specificity (1, 15). The authors discuss therefore their problems and suggest electrophysiological criteria of medium grade affections in the carpal tunnel syndrome which is the condition for compensation for occupational disease and which so far was defined only roughly in this country.

Central nervous system disease

Multiple sclerosis Multiple sclerosis (MS) is a chronic, inflammatory demyelinating disease, meaning that the myelin sheath of neurons is damaged. Symptoms of MS include visual and sensation problems, muscle weakness, numbness and tingling all over, muscle spasms, poor coordination, and depression. Also, patients with MS have reported extreme fatigue and dizziness, tremors, and bladder leakage. Myelopathy Myelopathy is an injury to the spinal cord due to severe compression that may result from trauma, congenital stenosis, degenerative disease or disc herniation. The spinal cord is a group of nerves housed inside the spine that runs almost its entire length. Tourette's

[An autopsy case with subacute spinal cord disease showing progressive paraplegia].

We report a 72-year-old woman who died of respitory failure. History included onset of diabetes mellitus at the age of 67 years and hypertension at the age of 72 years. The patient had been in good health otherwise until 2000, when she had onset of numbness or tingling of the bilateral lower limbs. On December 3, 2000, she was admitted to a hospital in the vicinity of her home because of the above-mentioned complaints. Neurological examinations revealed progressive paraplegia. Symptoms and signs suggested Guillain-Barré syndrome. Examinations of cerebrospinal fluids revealed cell count of 338/3 (mono 72%, poly 18%) and protein value of 100 mg/dl. Later the patient course deteriorated. On December 15, 2000, she was admitted to Hakujikai Memorial Hospital for the second time. Ten days later, MRI examination showed diffuse swelling of the spinal cord from the cervical (C 3/4) level to the thoracic level. Gd-enhanced T 1-weighted MRI performed 22 days later showed a partially enhanced lesion at the thoracic (Th 5/6) level of the spinal cord. The patient was treated with steroid therapy (methylprednisolone 500 mg/dl). She died of respiratory failure on January 6, 2001. The patient was presented in a neurological CPC. Neurological and imaging findings suggested a transverse myelopathy. However, there were several points in this case that were unusual for a typical transverse myelopathy, such as total sensory loss below spinal segments of thoracic level (Th 5) and motor weakness of the upper limbs of upper segment of the same level. A clinical neurologist concluded that the patient had subacute transverse myelopathy with fused multiple pathy pathologic lesions. We discussed whether this case was a transverse myelopathy or multiple sclerosis. Post mortem examination revealed acute necrotic myelopathy affecting the spinal cord from the second cervical to the tenth thoracic vertebrae, with conspicuous infiltration of CD 68-positive macrophages involving both gray and white matter, partially necrotic associated with scattered UCHL-1 dominants lymphocytic infiltration of T cells around vessels. There were relatively older lesions with demyelinating features in the spinal roots that were particularly dominant in the anterior roots. No demyelinated plaques in the optic chiasm, tracts and nerves, or in the cerebero-cerebellar white matter were found. Systemic pathological diagnosis was lung edema with fresh hemorrhage, pancreatic atrophy consistent with diabetes mellitus and choleductlithiasis.

Nerve conduction study

Repetitive nerve stimulation Interpretation of nerve conductions The interpretation of nerve conduction studies is complex and requires the expertise of health care practitioners such as clinical neurophysiologists, medical neurologists, physical therapists, chiropractic neurologists or physiatrists. In general, different pathological processes result in changes in latencies, motor, and/or sensory amplitudes, or slowing of the conduction velocities to differing degrees. For example, slowing of the NCV usually indicates there is damage to the myelin. Another example, slowing across the wrist for the motor and sensory latencies of the median nerve indicates focal compression of the median nerve at the wrist, called carpal tunnel syndrome. On the other hand, slowing of all nerve conductions in more than one limb indicates generalized diseased nerves, or generalized peripheral neuropathy. People with diabetes mellitus often develop generalized peripheral neuropathy.

Neuropathic arthropathy

Roughly 75% of patients experience pain, but it is less than what would be expected based on the severity of the clinical and radiographic findings. Pathogenesis Any condition resulting in decreased peripheral sensation, proprioception, and fine motor control: Diabetes mellitus neuropathy (the most common in the U.S. today, resulting in destruction of foot and ankle joints), with Charcot joints in 1/600-700 diabetics; related to long-term high blood glucose levels. Alcoholic neuropathy Cerebral palsy Leprosy Syphilis (tabes dorsalis), caused by the organism Treponema pallidum Spinal cord injury Myelomeningocele Syringomyelia Intra-articular steroid injections Congenital insensitivity to pain Peroneal muscular atrophy

[Left hand clumsiness due to disturbance of kinesthesia after damage to the dorsal column of the high cervical cord].

We described a 48-year-old, right-handed woman who manifested left hand clumsiness after damage to the dorsal column of the high cervical cord due to probable multiple sclerosis. On February 29, 1996, she developed a weakness in the right limbs. Subsequently, she suffered numbness and clumsiness in the left limbs, even though muscle strength of the left limbs was preserved. Seventeen days later, she was referred to our hospital. A T2-weighted MRI after admission demonstrated high signal intensities in the left dorsal column and the right antero-lateral part of the cervical cord at the C1 to C3 vertebral level. Under the diagnosis of probable multiple sclerosis, steroid pulse therapy was applied twice and she gradually regained muscle strength in the right limbs and sensation in the left limbs. One month later, elemental sensations such as pain, touch, temperature, vibration, and position, as well as discriminative sensations such as localization sensation, two-point discrimination, barognosis, pinch-press discrimination, and graphesthesia in the left limbs returned to normal. However, her left hand remained clumsy, especially when she tried to manipulate objects. She also showed a great difficulty in sustaining a constant level of pinching force by the left thumb and index finger, and in localizing her right thumb placed in space with the left hand with her eyes closed. She stated herself that she could not sense at all how her left hand and fingers were moving. Somatosensory evoked potentials recorded from the right scalp showed that the NI was poorly organized and the patency of subsequent peaks was delayed. Transcranial magnetic stimulation revealed that the pyramidal tract from the right motor cortex to the left cervical cord was functionally intact. These observations lead us to conclude as follows: (1) the patient's left hand clumsiness is probably due to the disturbance of kinesthesia, which is crucial to activate temporo-spatial patterns of complex hand and finger movements as well as to maintain long sequences of simple motor execution without vision; and (2) kinesthesia is a specific sensation that is presumably conveyed by the dorsal columns and could be selectively affected by a cervical cord lesion.

Distal hereditary motor neuropathy type V is a particular type of neuropathic disorder. In general, distal hereditary motor neuropathies affect the axons of distal motor neurons and are characterized by progressive weakness and atrophy of muscles of the extremities. It is common for them to be called "spinal forms of Charcot-Marie-Tooth disease (CMT)", because the diseases are closely related in symptoms and genetic cause. The diagnostic difference in these diseases is the presence of sensory loss in the extremities. There are seven classifications of dHMNs, each defined by patterns of inheritance, age of onset, severity, and muscle groups involved. Type V (sometimes notated as Type 5) is a disorder characterized by autosomal dominance, weakness of the upper limbs that is progressive and symmetrical, and atrophy of the small muscles of the hands.

Multiple myeloma

Neurological symptoms Some symptoms (e.g., weakness, confusion, and fatigue) may be due to anemia or hypercalcemia. Headache, visual changes, and retinopathy may be the result of hyperviscosity of the blood depending on the properties of the paraprotein. Finally, radicular pain, loss of bowel or bladder control (due to involvement of spinal cord leading to cord compression) or carpal tunnel syndrome, and other neuropathies (due to infiltration of peripheral nerves by amyloid) may occur. It may give rise to paraplegia in late-presenting cases. When the disease is well-controlled, neurological symptoms may result from current treatments, some of which may cause peripheral neuropathy, manifesting itself as numbness or pain in the hands, feet, and lower legs.

[Natural history of carpal tunnel syndrome--a review].

The review of the literature on the natural history of the carpal tunnel syndrome is presented. It is shown that the condition is characterised by non-uniform and unpredictable clinical course, in which besides the progressive type of evolution, a regressive one (characterised by spontaneous resolution of symptoms) and type of stable clinical picture (with episodes of exacerbation and resolution of symptoms) exist. Proportion of prevalence of particular types of clinical courses is not precisely estimated, but it appears that at least a half of the cases is of non-progressive type. Non-operative treatment of the condition may be effective in those particular cases, without risk of the development of severe neurological complications as a consequence of impairment of the median nerve. The evidence form analysed studies shows that in carpal tunnel syndrome, the clinical symptoms and signs and nerve conduction disturbances have different natural histories. Clinical features are subjected to greater temporal fluctuations than electrophysiological findings, and they frequently do not correlate one with another. There is not common opinion about efficacy of intervention in extreme carpal tunnel syndrome, characterised by severe conduction disturbances in electrophysiological tests and fixed neurological deficits, however surgical decompression of the carpal tunnel appears to be more promising than decline of the treatment. The natural history of the syndrome occurred in the course of other diseases (or conditions, e.g. pregnancy) is different, depending on the type of the disease itself. In the commonest systemic diseases associated with carpal tunnel syndrome, such as diabetes, hypothyroidism and rheumatoid arthritis, there is not common opinion about their prognostic effect on the natural course of the syndrome.

Hirayama's disease: an Italian single center experience and review of the literature.

Hirayama's disease (HD), is a benign, self-limited, motor neuron disease, characterized by asymmetric weakness and atrophy of one or both distal upper extremities. In the present study we report the clinical, electrophysiological and MRI features of a group of Italian patients, with review of the literature. Moreover we propose an optimized MRI protocol for patients with suspected or diagnosed HD in order to make an early diagnosis and a standardized follow up. Eight patients with clinical suspicion of Hirayama disease underwent evaluation between January 2007 and November 2013. All patients underwent standard nerve conduction studies (NCS), electromyography (EMG) and motor/sensory evoked potentials (MEP/SEP). Cervical spine MRI studies were conducted with a 1.5 Tesla MRI scanner in neutral and flexion position, including sagittal T1-weighted sequences and sagittal and axial T2-weighted sequences. The following diagnostic features were evaluated: abnormal cervical curvature, localized cervical cord atrophy in the lower tract (C4-C7), presence of cord flattening (CF), intramedullary signal hyperintensity on T2 weighted sequences, anterior shifting of the posterior wall of the cervical dural sac (ASD) and presence of flow voids (EFV) in the posterior epidural space during flexion. All patients complained of weakness in hand muscles as initial symptoms, associated with hand tremor in three of them and abnormal sweating of the hand palm in two of them. No sensory deficits and weakness at lower limbs were reported by any patients. Distal deep tendon reflexes at upper limbs were absent in all patients with the absence of the right tricipital reflex in one of them. Deep tendon reflexes at lower limbs were normal and no signs of pyramidal tract involvement were present. The clinical involvement at onset was unilateral in six patients (three left-sided and three right-sided) and bilateral asymmetric in two of them, with the right side more affected. With the progression of the disease all patients but one experienced weakness and wasting of hand muscles and forearm bilaterally, but still asymmetric. The duration of the progression phase of the disease ranged from eight months to three years. In all patients, NCS and EMG findings were consistent with a spinal metameric disorder involving the C7-T1 myotomes bilaterally; sensory conduction and electrophysiologic features at lower limbs were normal. MEP and SEP were normal and we did not observe the disappearance of the spinal potential during the neck flexion in any of the patients. MRI is the best diagnostic tool in the diagnosis of HD; it can confirm clinical diagnosis and exclude other conditions responsible for the neurological deficits leading to a correct patient management and therapy, limiting arm impairment. On MRI all patients had loss of the normal cervical lordosis (100%). Five patients had loss of attachment of posterior dural sac and anterior dural shift on flexion MRI with presence of flow voids from venous plexus congestion (62.5%); three patients had no anterior dislocation of the dural sac and no epidural vein congestion. Two patients showed localized cord atrophy, one at C5-C6 and the other at C6-C7 level (25%). Three patients had T2 intramedullary hyperintensities (37.5%) and cord flattening (CF) was present in 5 patients of 8 (62.5%). HD is a rare entity and a self-limited condition, but it has to be early differentiated from other diseases that may determine myelopathy and amyotrophy to establish a correct therapy and limit arm impairment. MRI is very important to confirm the clinical suspect of HD and a standardized MRI protocol using axial and sagittal images in both neutral and flexing position is needed, in order to diagnose and follow up affected patients.

Characteristics of nerve conduction studies in carpal tunnel syndrome.

Numerous nerve conduction tests are used for the electrodiagnosis of carpal tunnel syndrome (CTS), with a wide range of sensitivity and specificity reported for each test in clinical studies. The purpose of this study was to compare the diagnostic accuracy of various nerve conduction tests and determine the properties of the most accurate test. A prospective observational case control study. Eighty patients with clinically confirmed CTS and 80 asymptomatic healthy controls were included in the study. All patients underwent the routine hematological investigations as per the protocol. All cases and controls were subjected to various nerve conduction study protocols for CTS. Results were analyzed statistically. The two-tailed Student's t-test was used for the comparative statistical analysis. The sensitivity of each test was calculated as (the number of hands with an abnormal study result/the number of CTS hands) × 100. Comparison between percentages was performed by the McNemar test. The mean age was 38.19 ± 10.13 years and the female:male ratio was 1.5:1. The mean duration of disease was 0.89 ± 0.61 years. Hypothyroidism was present in 21 (26.25%) patients, whereas 13 (16.25%) and 4 (5%) patients had diabetes mellitus and rheumatoid arthritis, respectively. The median nerve motor latency was 4.73 ± 0.83 ms while the sensory latency was 3.44 ± 0.56 ms. The median nerve orthodomic sensory latency was found to be 2.57 ± 0.31 ms. The conduction velocity across the palm and wrist was 41.37 ± 0.67 ms. The sensitivity was the highest in the inching method (86.25%) and lowest for the conventional median motor and sensory latencies (56.25% and 45%, respectively). Addition of a single test of median and ulnar sensory latency, the median and radial sensory latency or the inching method, in routine protocol will improve the sensitivity for the diagnosis of CTS in all patients.

[A family of hereditary motor and sensory neuropathy type I with a mutation (Arg98-->His) in myelin Po--report on a second Japanese family].

A 46-year-old housewife had complaints of insidiously progressive muscle weakness and paresthesia in the distal lower limbs. On neurological examination, a slight to moderate degree of muscle weakness with slight atrophy was observed in the bilateral intrinsic hand muscles. A severe degree of muscle weakness with moderate atrophy was observed in tibialis anterior, gastrocnemius and soleus muscles. Muscle stretch reflexes were decreased in the upper limbs and absent in the lower limbs, without pathologic reflexes. She had a steppage gait. Vibratory sensation was slightly decreased in the hands and moderately decreased in the feet. Touch, pain and temperature sensations were also moderately decreased only in the feet. On laboratory examination, glycosuria (5.6g/dl) was noted. Fasting blood sugar was 226mg/dl with an elevated hemoglobin A1C level (12.7%). The right median motor and sensory nerve conduction velocities were 14.8 and 20.3 m/sec, respectively, with a markedly prolonged distal latency. No muscle action potential was obtained from stimulation of the right tibial nerve. Also, no nerve action potential was elicited from stimulation of the right sural nerve. A fascicular biopsy of the right sural nerve revealed the presence of both demyelinated and remyelinated axons, and an onion-bulb formation with a marked decrease in the density of the myelinated fibers. Based on the neurological examination and nerve conduction studies of the family members, a younger sister, younger brother and an elder daughter of the proband were found to be affected by demyelinating polyneuropathy. Diabetes mellitus was not found among the family members with laboratory evidences of demyelinating polyneuropathy. Based on the family history, an uncle on the mother's side of the proband, the proband's grandmother and a younger daughter of a proband's brother were considered to be affected. The uncle and grandmother had diabetes mellitus. Therefore, we concluded that this family had HMSN type I with autosomal dominant inheritance. In the studies on fluorescence in situ hybridization, and restriction fragment length polymorphism of the genomic DNA of the proband, a DNA duplication in the 17p11.2-12 region was not observed. However, the direct sequencing analysis of DNA fragments from genomic DNA encoding the Po gene of the proband revealed a substitution of histidine for arginine at the codon 98 in the extramembranous domain of Po. She was heterozygous for the mutant allele and normal allele. Alterations in the tertiary structure of the extramembranous domain of Po may result in an impairment of the peripheral myelin compaction. This is the second Japanese family with the same mutation (Arg98-->His) of myelin Po as reported previously by us, and this type of case is rare in the literature. Therefore, the mutation at the codon 98 may play a critical role in the development of the myelin abnormality in HMSN type IB.

Myelopathy

Presentation Clinical signs and symptoms depend on which spinal cord level (cervical, thoracic, or lumbar) is affected and the extent (anterior, posterior, or lateral) of the pathology, and may include: Upper motor neuron signs—weakness, spasticity, clumsiness, altered tonus, hyperreflexia and pathological reflexes, including Hoffmann's sign and inverted plantar reflex (positive Babinski sign) Lower motor neuron signs—weakness, clumsiness in the muscle group innervated at the level of spinal cord compromise, muscle atrophy, hyporeflexia, muscle hypotonicity or flaccidity, fasciculations Sensory deficits Bowel/bladder symptoms and sexual dysfunction Diagnosis

Neuroanatomy, Neurapraxia -- Clinical Significance

In these cases, a good knowledge of anatomy is beneficial. [4] The history should be thorough and the neurological examination, complete and meticulous, to obtain an accurate diagnosis and administer the appropriate management. Test for motor function and deranged sensation should include and follow specific nerve innervations. Depending on the nerve involved, neurologic findings include sensory impairment such as pain, allodynia, hyperesthesia, hypoesthesia, paresthesia, motor impairment such as weakness, atrophy in chronic cases, hyporeflexia. [4] Results of the neurologic examination serve to identify the type of injury, the location of the lesion, and the degree of injury of the sensory, motor, or both sensory-motor impairment, which is of prognostic value. [17] [18] [4] [22] Differential diagnosis includes peripheral neuropathies due to diabetes, hypothyroidism, alcohol, and malnutrition, radiculopathy, myelopathy, spinal cord trauma or infarction, muscle diseases. [18]

Neurogenic bladder dysfunction

Central nervous system Damage to the brain or spinal cord is the most common cause of neurogenic bladder. Damage to the brain can be caused by stroke, brain tumors, multiple sclerosis, Parkinson's disease or other neurodegenerative conditions. Bladder involvement is more likely if the damage is in the area of the pons. Damage to the spinal cord can be caused by traumatic injury, demyelinating disease, syringomyelia, cauda equina syndrome, or spina bifida. Spinal cord compression from herniated disks, tumor, or spinal stenosis can also result in neurogenic bladder. Peripheral nervous system Damage to the nerves that travel from the spinal cord to the bladder (peripheral nerves) can cause neurogenic bladder, usually the flaccid type. Nerve damage can be caused by diabetes, alcoholism, and vitamin B12 deficiency. Peripheral nerves can also be damaged as a complication of major surgery of the pelvis, such as for removal of tumors. Diagnosis

[Regarding the clinical diagnosis of the  monotopical  spinal forms of multiple sclerosis. The value of the fan sign in the adult].

We wish to discuss the value of the clinical history and examination in orientation of the diagnosis of probable multiple sclerosis (MS). We report the two year study of a woman who over the previous ten years had had three episodes of paraesthesia, with pins and needles in her left leg and other parts of the left side of her body, although never affecting head or neck. She also complained of tiring more than usual. In an outpatient clinic she was found to have a syndrome affecting the upper segments of the spinal cord, mainly involving the right side and resembling an incomplete Brown Sequard type syndrome. There were increased clinical muscle and deep reflexes. The most marked was that of the right deltoid (C5), bilateral fanning of the toes when the Babinski reflex was tested, Barré positive in the right leg, pins and needles and dysaesthesia on the left to an undetermined level. Function was well preserved when compared with the clinical signs found. The case was considered to be of monotopical MS. Spinal magnetic resonance findings confirmed the clinical diagnosis. We emphasise the value of careful clinical investigation directed towards the diagnosis of probable MS. We draw attention to the diagnostic value of the dissociation between the severe clinical alterations and the functional performance, which was surprisingly well maintained. Also we report the originality of the presence of bilateral fanning sign supporting the diagnosis of MS, occurring in a disease of adult life.

[Late diagnosed cervical myelomalesia in a case of Fahr disease experiencing a neuropathic pain].

Fahr disease is an idiopathic disorder characterized with deposition of calcium and a few other minerals in basal ganglia, cerebellum and subcortical brain area. A 51 years old female with the complaints of pain, numbness, tingling and weakness in both upper extremities for six months was referred to our electromyography laboratory with a suspicion of carpal tunnel syndrome. She got the diagnosis of Fahr disease upon the investigations for the convulsions that she experienced ten years ago. Beside, she had a generalized anxiety disoder. Neurological examination revealed mild to moderate weakness in flexion and extension of forearm, and extension of hand on both sides. She described dysesthesia on C6 & C7 dermatomes, bilaterally. Symmetric calsifications on both cerebellar hemispheres and basala ganglia were present on cranial CT. Median and ulnar nerve conduction studies were normal on both sides. Concentric needle electromyography revealed chronic neurogenic changes on the morphology of motor unit potentials recorded from the muscles of C6 & C7, bilaterally. Cervical magnetic resonance imaging revealed discopathies on C4-5, C5-6 and C6-7 levels causing myelomalacia. Neuropathic pain, paresthesia or muscle weakness on upper extremities are rare in Fahr disease. Presented case got the diagnosis of cervical discopathies in late as those findings were supposed to be related with Fahr disease. Therefore, clinicians should be aware of common findings occured during the course of this disease, and consider the possible coincidental pathologies when the atypical neurological deficits are observed in these patients.

Neurological diagnosis: aspects of bedside and electrodiagnostic examinations in relation to hand-arm vibration syndrome.

The objective of this paper, was to direct attention to the diagnostic strategy and clinical approach necessary in the diagnosis of neuropathy in workers exposed to vibration. The purpose encompassed evaluation of selected aspects of bedside and electrodiagnostic examinations with respect to biological validity and the ability to distinguish between subjects with and without neuropathy. The neurological examinations viewed were restricted to those applicable to the upper extremity and neck system. A MEDLINE search was performed through the clinical queries service of PubMed searching for the following terms: nerve-conduction, Tinel's test, Phalen's test, tendon reflex, two-point discrimination test, abduction external rotation test, and Spurling test. Retrieved articles were discussed both in relation to the test accuracy and the validity aspects of the tests. The evidence in support of the view that neurological tests can accurately distinguish between subjects with and without neuropathy specifically addressing hand-arm vibration syndrome was sparse. The initial number of diagnostic hypotheses could be reduced by progressively ruling out diseases based on negative results of highly sensitive tests. As the possible diagnostic alternatives become fewer, the use of positive results from highly specific tests are more effective. The information value of the various diagnostic tests is determined by the change in pre-test to post-test probability of target disorder, which depends on the prevalence of the disorder and the likelihood ratios of the tests. The review showed that target disease characteristics influence the test outcome as well as the choice of "gold standard" and the population domain of the studies. The selection of various bedside examinations and diagnostic electrophysiological tests should be dependent on the clinical context, the history and results from the successive diagnostic tests.