A 32-year-old male, a driver by occupation, initially presented to the psychiatry emergency services and he was subsequently referred to the neurology emergency services. The patient was accompanied by his wife, who gave the history of involuntary movements of the face and mouth for 1 month along with abnormal vocalizations. There were no specific aggravating and alleviating factors. Past history revealed the presence of fever and altered sensorium 4 years ago, which had lasted for approximately 2 weeks, and he had one episode of generalized tonic-clonic seizure during that time. Additionally, there were significant behavioral changes characterized by anger outbursts, irritability, and apathy since the last 4-5 years. There was no history of tremor, jerks, imbalance while walking, and abnormal posturing of any other body parts. There was no clear history of any intravenous drug abuse, toxin exposure, and head injury. None of his family members had history of tremor, parkinsonism, memory disturbance, or psychiatric disorders.
On the day of clinical evaluation, he was conscious, and alert, but was not completely cooperative for the physical examination. There were intermittent abnormal vocalizations. There was no neck rigidity suggestive of meningitis. All the cranial nerves were normal on examination, but he had absent light and accommodation reflex. Positive findings during the motor system examination were dominated by involuntary movements in the form of frequent opening and closing of the mouth, continuous perioral movement (chewing movements), and occasional protrusion of the tongue. He also had occasional ballistic hand movements. Rigidity and bradykinesia were minimal in both upper and lower limbs. All the deep tendon reflexes were well elicited and the plantars had flexor response in both sides. We did not find any cerebellar and sensory deficits and his gait was grossly normal (Video 1).
Routine hemogram and biochemical parameters were within normal limits. Considering the fact that subacute onset involuntary movements could be secondary to structural lesions, magnetic resonance imaging (MRI) of the brain was done, which revealed significant bilateral temporal lobe atrophy and signal changes in the thalamus and basal ganglia (Figure 1). The possibility of chronic neuroinfection was considered as the patient had a history of altered sensorium 5 years previously, and there had been behavioral changes over 4-5 years. Infections with human immunodeficiency virus (HIV), herpes simplex virus (HSV), and syphilis were considered. Subsequent examinations revealed that HIV was negative and the cerebrospinal fluid (CSF) profile did not reveal any convincing evidence of bacterial or viral meningitis (cell count, 7 polymorphonuclear leucocytes/mL; protein, 56 mg/dL, and glucose, 84 mg/dL). After ruling out these two common infections (HIV and HSV), which may present with neuropsychiatric symptoms, we checked the serum for Veneral Disease Research Laboratory (VDRL) and Treponema Pallidum Heamagglutination (TPHA): they were both positive in this case. CSF was non-reactive for VDRL as it may happen in ~50% of patients with neurosyphilis (~50%). Estimation of immunoglobulin G in CSF and a test for rapid plasma reagin could not be done, as these tests are not available in our center. A diagnosis of neurosyphilis was established in this case for the following reasons: (1) subacute onset neuropsychiatric symptoms, (2) MRI changes that are commonly observed in neurosyphilis, (3) CSF pleocytosis, and a mild rise in CSF protein, and (4) serum reactive to both VDRL and TPHA. The diagnosis gained further support from the fact that the patient had notable improvement in both motor and behavioral symptoms after 6 weeks of treatment with penicillin.