The Parkinson's-Reversing Breakthrough

What is Parkinsons Disease

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Abbreviations: CBD, corticobasal degeneration; DLB, dementia with Lewy bodies; MSA, multiple system atrophy; OPCA, olivopontocerebellar atrophy; PD, Parkinson's disease; PSP, progressive supranuclear palsy; SND, striatonigral degeneration.

Abbreviations: CBD, corticobasal degeneration; DLB, dementia with Lewy bodies; MSA, multiple system atrophy; OPCA, olivopontocerebellar atrophy; PD, Parkinson's disease; PSP, progressive supranuclear palsy; SND, striatonigral degeneration.

Toxin-Induced Parkinsonism

In general, these disorders are uncommon and may pose less of a differential diagnostic problem. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism is distinct from the dopamine-blocking agent induced parkinsonism in that it is irreversible and is due to the destruction of the substantia nigra neurons (73). The clinical features have some similarities to PD except that the onset is abrupt and the affected individuals are younger than typical PD (74,75). These patients respond to levodopa with early levodopa-induced fluctuations (76). The patients may worsen gradually even in the absence of continued exposure to the toxin (77). In manganese poisoning, patients may superficially resemble PD, their symptoms including soft speech, clumsiness, and impaired dexterity; however, they have a peculiar cock-walk gait in which they swagger on their toes (78,79). The typical rest tremor is absent. They may also have limb and truncal dystonia that is very unusual in untreated PD. Dementia and psychosis may occur, and these patients do not respond well to dopaminergic drugs. Manganese is a component of welding rods, and welders have been said to develop typical PD at an earlier age of onset as compared to controls (80). However, many studies fail to show a relationship between welding and PD (81).

Parkinsonism as a result of carbon monoxide intoxication has been well described (82). The parkinsonism may be delayed after the acute episode. These patients often show a slow shuffling gait, loss of arm swing, retropulsion, bradyki-nesia, rigidity and, occasionally, a rest tremor. The pull test tends to be markedly abnormal. A CT scan or MRI may show necrotic lesions of the globus pallidus (83,84). There may also be associated white matter lesions that may progress without further exposure to carbon monoxide (85). Other toxins that have been reported to cause parkinsonism include carbon disulfide (86), cyanide (87,88), and methanol (89,90). These patients often have an acute onset and, in some cases, show basal ganglia lesions on neuroimaging. Post-hypoxic parkinsonism has an acute evolution following a bout of severe prolonged hypoxia. Variable degrees of intellectual deterioration often accompany post-hypoxic parkinsonism, and the patients usually do not have rest tremor.

Post-Traumatic Parkinsonism

Isolated head trauma is rarely a cause of parkinsonism (91). Parkinsonism may be seen in the setting of diffuse severe cerebral damage after severe brain injury (92). However, repeated minor trauma to the head as in boxers (dementia pugilistica) may be complicated by the late onset of dementia, parkinsonism, and other clinical features (93,94). Boxers are not immune to developing typical PD; however, the onset of parkinsonism and dementia in a boxer would be suggestive of dementia pugulis-tica. Imaging studies may show a cavum septum pellucidum and cerebral atrophy. A PET study using 6-fluorodopa showed damage to the caudate and the putamen in post-traumatic parkinsonism, whereas in PD the putamen is more severely involved.

Multi-Infarct Parkinsonism

Arteriosclerotic or multi-infarct parkinsonism is a debatable entity (95). However, patients who have predominant gait disturbance with slightly wide-based gait with some features of gait apraxia and frequent freezing are seen (96). These patients are labeled lower-half parkinsonism, and they usually lack the typical rest tremor or other signs in the upper extremities (97). The gait disorder may not be distinct from senile gait, and a similar gait disorder may also be seen in patients with Bin-swanger's disease (98,99). Levodopa responsiveness is uncommon but has been demonstrated occasionally in patients with pathologically confirmed multi-infarct parkinsonism.

The proposed criteria for the diagnosis of vascular parkinsonism include acute or subacute onset with a stepwise evolution of akinesia and rigidity along with vascular risk factors (100). This should be supplemented by at least two or more infarcts in the basal ganglia on neuroimaging. In some cases, there may be more widespread MRI white matter abnormalities. Spontaneous improvement in symptoms and signs without dopaminergic therapy is suggestive of vascular parkinsonism.

Some patients with multiple cerebral infarction have a clinical picture characterized by gaze palsies, akinesia, and balance difficulties consistent with PSP. In fact, one study found that 19 out of 58 patients with a clinical diagnosis of PSP had radiographic evidence of multiple small infarcts in the deep white matter and the brainstem (35).

Parkinsonism with Hydrocephalus

Varying degrees of hypomimia, bradykinesia, and rigidity in the absence of tremor may occur in high pressure as well as in normal pressure hydrocephalus (NPH)

(101). High-pressure hydrocephalus rarely poses any diagnostic difficulties because of the relatively acute onset in the presence of signs of raised intracranial pressure. However, NPH may be more difficult to distinguish from PD. The classic triad of NPH includes a subacute onset of dementia, gait difficulty, and urinary incontinence

(102). The gait is slightly wide-based, with features of gait apraxia or slight ataxia. Rarely, levodopa responsiveness has been demonstrated (103). In some patients, the gait might improve for a few hours to days by the removal of CSF (104).

Parkinsonism Due to Structural Lesions of the Brain

Blocq and Marinesco were the first to report a clinicopathological correlation of midbrain tuberculoma, involving the nigra and contralateral parkinsonism (105,106). In most cases, the responsible lesions have been tumors, chiefly gliomas and menin-giomas. Interestingly, these are uncommon in the striatum and have usually involved the frontal or parietal lobes. Subdural hematoma may present with subacute onset of parkinsonism with some pyramidal signs (107). Other rare causes of parkinsonism and structural lesions have included striatal abscesses (108) and vascular malformations. However, the structural lesions are easily confirmed by neuroimaging. Occasionally, parkinsonism has been reported in patients with basal ganglia calcifications that usually occur in the setting of primary hypoparathyroidism. The calcification should be obvious on neuroimaging (109).

Infectious and Postinfectious Causes of Parkinsonism

The classic postencephalitic parkinsonism is not seen currently. It was characterized by a combination of parkinsonism and other movement disorders. Particularly, characteristics were "oculogyric crises", which resulted in forceful and painful ocular deviation lasting minutes to hours. Other causes of oculogyric crises are Tourette's syndrome, neuroleptic-induced acute dystonia, paroxysmal attacks in multiple sclerosis, and possibly conversion reaction. The parkinsonism may improve with lev-odopa but response deteriorates quickly. Parkinsonism rarely occurs as a sequelae of other sporadic encephalitides. Human immunodeficiency virus dementia has also been reported with parkinsonian features. Other infectious causes include striatal abscesses and neurosyphilis.

Psychogenic Parkinsonism

As compared to other psychogenic movement disorders such as tremor, psychogenic parkinsonism is uncommon (110). A tremor of varying rates with marked dis-tractibility along with inconsistent slowness and the presence of feigned weakness and numbness might lead to the correct diagnosis.

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