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PubMed1996

Extrapyramidal motor signs in clinically diagnosed Alzheimer disease.

We reviewed clinical case series published over a 10-year period addressing the cross-sectional frequency, incidence, and diagnostic and prognostic significance of extrapyramidal signs (EPS) in Alzheimer disease (AD). The review was prompted by recent reports of Lewy body (LB) pathology in the brains of many AD patients and the association of LB pathology with clinical parkinsonism in AD. In the clinical case series reviewed, we evaluated several possible determinants of prevalent EPS, including neuroleptic use, EPS assessment technique, and dementia severity. Neuroleptics were a well recognized cause of parkinsonism in these reports, though some failed to document the frequency of neuroleptic use. Assessment methods were also important: Studies using structured clinical research scales to rate EPS reported higher frequencies than studies employing routine neurological examination. The relationship between parkinsonism and dementia severity was complex. Some studies found bradykinesia, facial masking, and parkinsonian postural changes even in mildly demented, neuroleptic-naive AD patients. Rigidity, on the other hand, became increasingly common as dementia progressed. AD patients with EPS showed faster cognitive and functional decline and earlier death than those without EPS, even after consideration of differences in initial dementia severity. In the differential diagnosis of dementia with parkinsonism, LB disease in its various forms, including AD with LB, is the principal diagnostic consideration. Future studies of parkinsonism in AD should employ standardized clinical rating scales and should exclude patients on neuroleptics or analyze their results separately. Investigators should report frequencies for individual parkinsonian signs in addition to the overall prevalence of EPS to facilitate meaningful comparisons across studies.

Alzheimer Disease↗
PubMed1981

Drug-induced extrapyramidal disorders - a neuropsychiatric interface.

In psychiatric literature, the term extrapyramidal syndrome has traditionally encompassed a wide variety of drug-induced movement disorders. Recently, it has become increasingly clear that the natural history, pathophysiology, and pharmacology of individual movement disorders are distinct, making this unifying term obsolete and, in fact, a source of confusion. The topic of drug-induced movement disorders is reviewed, and a classification system based on anatomy, pharmacology, and therapeutic considerations is discussed.

Antipsychotic Agents↗
PubMed1995

Essential tremor and its variants.

Essential tremor is the commonest of movement disorders. Although sometimes prefaced with the term 'benign', it often causes significant disability. Diagnosis is based on the clinical finding of a postural tremor, predominantly affecting the upper limbs, that is absent at rest and not associated with extrapyramidal or cerebellar signs. There are, as yet, no specific anatomical, physiological, biochemical or genetic markers for the condition. Postural limb tremors, clinically indistinguishable from essential tremor, may occur in patients who have, or will later develop, other neurological conditions; whether such patients have essential tremor is a matter of controversy that will only be resolved with a better understanding of the pathophysiology of essential tremor. Positron emission tomography in patients with essential tremor reveals increased cerebellar activity even at rest, a finding that is consistent with the cerebellum having an important role in the generation of tremor. Abnormal cerebellar function has also been invoked to account for the abnormal manner in which patients with essential tremor perform rapid voluntary wrist movements. Molecular genetic studies in hereditary essential tremor have been initiated, but with negative results so far. Several new drug treatments have been tried, but with limited success; the role of thalamic stimulation and botulinum toxin in the treatment of essential tremor remains to be judged.

Cerebellum↗
PubMed2006

Apparent transient effects of recent "ecstasy" use on cognitive performance and extrapyramidal signs in human subjects.

OBJECTIVES: Our purpose is to investigate cognitive performance and extrapyramidal function early after ecstasy use. BACKGROUND: Ecstasy, containing 3,4 methylenedioxymethamphetamine, has shown evidence of causing cognitive deficits and parkinsonian signs. Previous research has examined cognitive performance after a period of prolonged abstinence, but research assessing the early effects of ecstasy after recent use is limited despite temporal neurochemical differences demonstrated in nonhuman models. METHODS: This study compared task performance between 13 ecstasy users (10 to 15 h postdrug use) and a control group on a battery of neuropsychologic assessments while matching for education level, sleep deprivation, and premorbid IQ. The groups were also compared on measures relating to parkinsonian signs. RESULTS: The ecstasy subjects showed impairments on measures of executive function as evaluated by Raven's Standard Progressive Matrices (SPM) and the Wisconsin Card Sorting Task (WCST). Short-delay free recall memory was also impaired in ecstasy subjects on the California Verbal Learning Test (CVLT-II). No extrapyramidal motor impairments were detected. CONCLUSIONS: These deficits resemble deficits previously reported in chronic ecstasy use but also seem to reveal transient impairments in executive function. Future research is needed to better understand the neurologic and neuropsychologic implications of ecstasy use across time and extent of use.

Adult↗
PubMed1979

Paroxysmal hemipareses in childhood.

The authors report three patients suffering since infancy from transient attacks of paresis. The flaccid pareses most frequently affect the extremities in a hemiplegic fashion, but occasionally there is monoparesis or quadriparesis. The laterality and degree of the paresis are variable. Conciousness is always preserved, and in two cases attacks were preceded by ocular motor disturbances (skew deviation, nystagmoid jerks and conjugate deviations). Exceptionally, the transient hemiparesis may be preceded by a grand mal epileptic fit, though they are more likely to appear sporadically and independently of the paretic changes. In the interparoxysmal periods the children showed pronounced hypotonia, hyperkinetic extrapyramidal features and oligophrenia. Neuroradiological procedures have excluded brain anomalies of vascular or other aetiology and simple biochemical analyses were negative. EMG during paretic periods have revealed central motor neuron lesions, while EEG demonstrated non-specific paroxysmal features. A brain-stem dysfunction in the aetiology is postulated.

Adolescent↗