future possibility for definitive clinical diagnosis prior to death. however, despite their benefits, information learned from mri and spect during the beginning of cbd progression tend to show no irregularities that would indicate the presence of such a neurodegenerative disease. fdopa pet is used to study the efficacy of the dopamine pathway. despite the undoubted presence of cortical atrophy (as determined through mri and spect) in individuals experiencing the symptoms of cbd, this is not an exclusive indicator for the disease. thus, the utilization of this factor in the diagnosis of cbd should be used only in combination with other clinically present dysfunctions. mri mri images are useful in displaying atrophied portions of neuroanatomical positions within the brain. as a result, it is especially effective in identifying regions within different areas of the brain that have been negatively affected due to the complications associated with cbd. to be specific, mri of cbd typically shows posterior parietal and frontal cortical atrophy with unequal representation in corresponding sides. in addition, atrophy has been noted in the corpus callosum. functional mri (fmri) has been used to evaluate the activation patterns in various regions of the brain of individuals affected with cbd. upon the performance of simple finger motor tasks, subjects with cbd experienced lower levels of activity in the parietal cortex, sensorimotor cortex, and supplementary motor cortex than those individuals tested in a control group. spect spect is currently being used to try to detect cbd. with many patients of cbd, there are areas in the basal ganglia which have difficulties receiving dopamine, typically asymmetrically. specifically affected, are dopamine transporters which are presynaptic on the nigrostriatal cells. spect is used to detect these abnormalities in dopamine transporters. given that many patients have asymmetrical loss of function and metabolism this can help differentiate patients with cbd and those with alzheimer's. spect studies of individuals diagnosed with cbd involve perfusion analysis throughout the parts of the brain. spect evaluation through perfusion observation consists of monitoring blood release into different locations in tissue or organ regions, which, in the case of cbd, pertains to localized areas within the brain. tissue can be characterized as experiencing overperfusion, underperfusion, hypoperfusion, or hyperperfusion. overperfusion and underperfusion relate to a comparison with the overall perfusion levels within the entire body, whereas hypoperfusion and hyperperfusion are calculated in comparison to the blood flow requirements of the tissue in question. in general, the measurements taken for cbd using spect are referred to as regional cerebral blood flow (rcbf). in general, spect reveals hypoperfusion within both the posterior regions of the frontal and parietal lobes. as in images gathered through mri, spect images indicated asymmetry in the presentation of abnormalities throughout the brain. additional studies have revealed the presence of perfusion anomalies in the thalamus, temporal cortex, basal ganglia, and pontocerebellar (from the pons to the cerebellum) locations within subjects' brains. fdopa pet research has suggested that the integrity of the dopamine system in the striatum has been damaged as an effect of cbd. current studies employing the use of fdopa pet scanning (fdopa pet) as a possible method for identifying cbd have focused on analyzing the efficiency of neurons in the striatum that utilize the neurotransmitter dopamine. these studies have concluded that, in general, dopamine uptake was diminished in the caudate and the putamen. this characteristic also has the potential to be useful in distinguishing cbd from the similar pd, as individuals having been diagnosed with pd were more likely to have a lower uptake of dopamine than in individuals with cbd. other clinical tests or procedures that monitor the presence of dopamine within the brain (β-cit spect and ibzm spect) have shown similar findings. β-cit serves as an indicator for presynaptic dopaminergic neurons, whereas ibzm is a tracer that shows an affinity for the postsynaptic neurons of the same type. despite agreement with other imaging studies, these two spect methods suffer some scrutiny due to better accuracy in other imaging methods. however, β-cit spect has proven to be helpful in distinguishing cbd from psp and multiple system atrophy (msa). corticobasal syndrome main article: corticobasal syndrome all of the disorders and dysfunctions associated with cbd can often be categorized into a class of symptoms that present with the disease of cbd. these symptoms that aid in clinical diagnosis are collectively referred to as corticobasal syndrome (cbs) or corticobasal degeneration syndrome (cbds). alzheimer's disease, pick's disease, ftdp-17 and progressive supranuclear palsy can display a corticobasal syndrome. it has been suggested that the nomenclature of corticobasal degeneration only be used for naming the disease after it has received verification through postmortem analysis of the neuropathology. cbs patients with greater temporoparietal degeneration are more likely to have ad pathology as opposed to frontotemporal lobar degeneration. treatment because the exact cause of cbd is unknown, there exists no formal treatment for the disease. instead, treatments focus on minimizing the appearance or effect of the symptoms resulting from cbd. the most easily treatable symptom of cbd is parkinsonism, and the most common form of treatment for this symptom is the application of dopaminergic drugs. however, in general only moderate improvement is seen and the relief from the symptom is not long-lasting. in addition, palliative therapies, including the implementation of wheelchairs, speech therapy, and feeding techniques, are often used to alleviate many of the symptoms that show no improvement with drug administration. there is no consensus on what causes cbd and so most of the treatment goes in helping symptoms. many treatments have low success rates or have not been tested thoroughly or produced frequently. for example, in relation to the motor aspect of disability, cbd has a high resistance against treatments to help the dopamine intake like levodopa. a number of studies have reported no real levels of improvement based with the use of similar drugs/dopaminergic agonists. because of the brains levels of inhibition, some medications have focused on creating an inhibition that would negate the effect. many of these relaxants and anticonvulsants have some success but also have unwanted side effects. cognitive and associative effects of cbd are also hard to treat as we are still unsure of many of the treatments for the symptomatic diseases that ensue like dementia, aphasia, neglect, apraxia and others. epidemiology clinical presentation of cbd usually does not occur until age 60, with the earliest recorded diagnosis and subsequent postmortem verification being age 28. although men and women present with the disease, some analysis has shown a predominant appearance of cbd in women. current calculations suggest that the prevalence of cbd is approximately 4.9 to 7.3 per 100,000 people. the prognosis for an individual diagnosed with cbd is death within approximately eight years, although some patients have been diagnosed over 17 years ago (2017) and are still in relatively good standing, but with serious debilitation such as dysphagia, and overall limb rigidity. the partial (or total) use of a feeding tube may be necessary and will help prevent aspiration pneumonia, primary cause of death in cbd. incontinence is common, as patients often can't express their need to go, due to eventual loss of speech. therefore, proper hygiene is mandatory to prevent urinary tract infections. cbd research has been limited by the rarity of the disease and the lack of research criteria. it is estimated to affect 0.6-0.9 per 100,000 per year. progressive supranuclear palsy (psp) without cbd is estimated to be ten times more common. cbd represents roughly 4–6% of patients with parkinsonism. average age at disease onset is about 64, with the youngest confirmed onset being at age 43. there may be a slight female predominance. history corticobasal syndrome was first recognized in 1967 when rebeiz, kolodny, and richardson jr described three people with a progressive asymmetric akinetic-rigid syndrome combined with apraxia, which they named corticodentatonigral degeneration with neuronal achromasia. the condition was "mostly forgotten" until 1989, when marsden et al. used the name corticobasal degeneration. in 1989 gibb and colleagues provided detailed clinical and pathological descriptions in a further three cases adopting the name corticobasal degeneration, after which various other names included "corticonigral degeneration with nuclear achromasia" and "cortical basal ganglionic degeneration". although the underlying cause of cbd is unknown, the disease occurs as a result of damage to the basal ganglia, specifically marked by neuronal degeneration or depigmentation (loss of melanin in a neuron) in the substantia nigra. additional distinguishing neurological features of those diagnosed with cbd consist of asymmetric atrophy of the frontal and parietal cortical regions of the brain. postmortem studies of patients diagnosed with cbd indicate that histological attributes often involve ballooning of neurons, gliosis, and tauopathy. much of the pioneering advancements and research performed on cbd has been completed within the past decade or so, due to the relatively recent formal recognition of the disease. the office of rare diseases in the united states created the first criteria in 2002, and the armstrong clinical diagnostic criteria were created in 2013. society and culture the salt path by raynor winn is an inspiring account of walking england's 630 mile south west coast path with her husband who had corticobasal degeneration.