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PubMed2000

Parkinsonism as an initial manifestation of brain tumor.

Parkinsonism secondary to neoplasm is uncommon. We report two patients with bilaterally symmetric parkinsonism as the initial presentation of their brain tumors. The first patient was a 71-year-old woman who presented with a gradual onset of bilateral resting tremor, bradykinesia and rigidity. Computerized tomography (CT) of the brain revealed a large parasagittal tumor in the left frontal lobe. The patient completely recovered from the parkinsonian symptoms after removal of the brain tumor. The second patient, a 74-year-old man with a history of renal cell carcinoma of the right kidney suffered from an insidious onset of bilateral bradykinesia, rigidity and gait difficulty. Cerebral metastasis was noted on the brain CT scan. Early recognition of intracranial tumor as the cause of parkinsonism is important for the management of this type of movement disorder. Moreover, brain CT scanning plays an important role in the differential diagnosis of patients with parkinsonian symptoms.

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PubMed1991

Short-latency autogenic inhibition in patients with Parkinsonian rigidity.

The spinal Ib interneuron efficacy has been compared in 11 control subjects and 19 patients with parkinsonian rigidity. In normal subjects, gastrocnemius medialis nerve stimulation induces an inhibition of the soleus H reflex for 3 to 8 msec with a peak at 5 msec of 83.72 +/- 7.28% of the control value of H reflex. In parkinsonian patients, inhibition is reduced or even replaced by facilitation, which also peaks at 5 msec. The departures from normal values correlate with rigidity intensity assessed by the Webster scale. Increase in rigidity is associated, first, with a reduction of inhibition and, from a score of 2 or more, with facilitation replacing the normal inhibition. In addition to providing an electrophysiological index of rigidity, reduction in autogenic inhibition might be one of the neurophysiological mechanisms underlying rigidity. In association with the known hyperactivity of the Ia inhibitory interneuron in Parkinson's disease, reduction of activity of Ib interneuron could be explained by an increased activity in the reticularis gigantocellularis nucleus; its efferent tracts both inhibit Ib interneurons and activate Ia interneurons.

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PubMed1993

Akinetic-rigid syndrome in a 13-year-old girl with HIV-related progressive multifocal leukoencephalopathy.

A 13-year-old HIV-infected girl presented with a rapidly progressive akinetic-rigid syndrome. Cranial magnetic resonance imaging revealed bilateral centrum semiovale lesions extending into the basal ganglia. Detailed histopathological study of a biopsy specimen from the involved regions resulted in a diagnosis of progressive multifocal leukoencephalopathy (PML). This case illustrates that an akinetic-rigid syndrome may be a rare presentation of PML. HIV-related PML may have unusual radiological features. Brain biopsy may be necessary to confirm PML in cases associated with atypical clinical and radiological presentations.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

Treatment of parkinsonian syndromes in developing countries.

Parkinsonism is the commonest extrapyramidal disorder. The condition arises when the striatonigral dopamine content falls below a critical value. The principle of treatment is dopamine replacement or counteracting the effects of acetycholine, the neurotransmitter which is in abundance. The choice of drug is determined by availability, cost, and side effects. The most commonly prescribed drugs in developing countries are the anticholinergics, which are the least expensive. The dopamine-replacement agents are second-line drugs and it appears as if low doses are effective in improving rigidity, gait abnormality, and postural instability. The use of dopa-agonist drugs is more limited, because of cost and side effects. Surgical management of cases is still in its infancy in developing countries. This review also highlights the more recent modes of management practised mainly in developed countries.

Acetylcholine↗
PubMed1984

Recent physiological and pathophysiological aspects of Parkinsonian movement disorders.

Deficits in the neural control of limb movements constitute a major part of Parkinsonian symptoms and are linked to a decay of dopaminergic neurotransmission. In animal models, Parkinsonian-like hypokinesia is consistently reproduced with large nigrostriatal dopamine depletions, while tremor and rigidity are less readily obtained. Lesions leading to a less than 70% striatal dopamine depletion are largely compensated by an increased activity of dopamine terminals. With more important lesions, supersensitivity of striatal non-adenylate cyclase-linked dopamine receptors occurs. Electrophysiological studies in Parkinsonian patients demonstrate increased reaction times and a reduced build-up of movement-related muscular activity underlying hypokinesia and provide circumstantial evidence for a central origin of tremor and rigidity. Single cell activity in unlesioned, behaving monkeys shows an increasingly direct relationship to movements when following the neural connections from mid-brain dopamine cells via striatum, globus pallidus, thalamus to pyramidal tract neurons of motor cortex. These data corroborate experimentally the concept that Parkinsonian hypokinesia is due to a failure of basic behavioral activating mechanisms.

Animals↗
PubMed2002

Progression of gait disorder and rigidity and risk of death in older persons.

BACKGROUND: Bradykinesia, gait disturbance, rigidity, and tremor are common motor signs in old age. All of these signs are associated with increased morbidity and mortality, but the extent to which they are progressive is unknown. METHODS: Study participants were 787 older Catholic clergy members without clinically diagnosed PD, related conditions, or dementia at baseline. They were evaluated annually for up to 7 years, with >95% follow-up participation by survivors. Evaluations included administration of a modified version of the motor portion of the Unified PD Rating Scale (UPDRS), from which previously established measures of the global UPDRS and four specific motor signs were derived. Scores represent the percent of the total possible UPDRS score obtained. RESULTS: At baseline, the global UPDRS score ranged from 0 to 36.3 (mean +/- SD, 7.3 +/- 6.4). It increased by an average of 0.69 unit per year during follow-up, with more rapid progression in older persons, but there was wide variability with no progression in 21% of subjects and annual increases of up to 8.23 units in the remaining 79%. Of 129 persons who died, 106 had follow-up UPDRS data. In a proportional hazards model, risk of death was associated with both the level of the global UPDRS score at baseline and the annual rate of progression (both p < 0.001). Overall, risk of death in subjects who had some worsening of the global UPDRS score was 2.93 times the rate among those without progression (95% CI, 1.32-6.50). Gait disorder/postural reflex impairment and rigidity worsened, but bradykinesia and tremor did not. Risk of death was associated with worsening of gait/posture but not with the other signs. CONCLUSION: Gait disorder and rigidity, as assessed with the modified UPDRS, are usually progressive in old age. Both the severity of the gait disorder and its rate of progression are strongly associated with risk of death.

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PubMedDate not supplied

[Extrapyramidal signs in Alzheimer's disease].

Extrapyramidal signs were assessed in 112 patients satisfying NINCDS/ADRDA criteria for probable Alzheimer's disease. They were present in 50% of the patients. The most common features of them were bradykinesia and rigidity. Resting tremor was rarely encountered. There were no significant differences in age of onset, symptom duration, presence of primitive reflexes and psychotic symptoms between cases with and without extrapyramidal signs, while the presence of extrapyramidal signs was associated with statistically significant greater dementia severity.

Age of Onset↗
PubMed1982

[Extrapyramidal rigidity with dystonia, optic atrophy and bilateral putaminal lesions in an adolescent. Juvenile form of Leigh's disease (author's transl)].

A 19-year-old man presented with an apparently non-familial neurological disorder that had progressed from the age of 6 years. Dystonia of the trunk and limbs with extrapyramidal rigidity, dysarthria, a pyramidal syndrome with spasticity of the lower limbs, bilateral optic atrophy, and nystagmiform ocular movements were present. CT scan demonstrated symmetrical putaminal lesions. The different aetiologies of bilateral striatal lesions are considered, the final diagnosis being a juvenile form of Leigh's disease.

Adult↗
PubMed1983

Stiff-man syndrome and dementia.

Stiff-man syndrome is characterized clinically by fluctuating muscular stiffness and spasm, and electromyographically by continuous motor unit activity at rest, which is abolished by sleep, general anesthesia, nerve block, curare, and several centrally-acting medications. A spinal or supraspinal origin has been proposed for this disorder. Some clinical and electrophysiologic features, along with an occasional association with encephalopathy, may support a proposed supraspinal cause. An elderly man with progressive dementia and concomitant development of stiff-man syndrome is described. He had not had stiff-man syndrome one year earlier, when he had only mild dementia. An association between stiff-man syndrome and dementia has not been previously described. Increased muscle tone and muscular rigidity is frequently encountered in patients with dementia, however, and pathologic reflexes involving neck and proximal musculature have been described in dementia. It is possible that this patient represents an exaggerated form of such motor disturbances in dementia, and that clinical and electromyographic features of stiff-man syndrome may be present with increased incidence in patients with dementia.

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PubMed1984

Defective utilization of sensory input as the basis for bradykinesia, rigidity and decreased movement repertoire in Parkinson's disease: a hypothesis.

From a review of the anatomical relationships and single unit activity in the components of the basal ganglia related to limb movement, it is concluded that the major outflow from basal ganglia circuits is via the motor cortex (area 4). Recent results of recording from area 4 neurons revealed that they preferentially "encode" the higher derivatives of movement, i.e. acceleration and jerk. In the parkinsonian (PK) patient and in the monkeys treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), EMG responses to imposed loads show a markedly increased gain of the "M2" component which depends upon the integrity of area 4 and which correlates with the severity of PK rigidity. The above observations are considered, along with those of others (demonstrating prolonged movement times, a decreased "repertoire" of voluntary movements fractionation of voluntary movements, inability in tracking movements without visual input, and failure to improve performance in PK's) in relation to a model of the interactions between sensory input and motor programs. Using this model, it is hypothesized that the above PK movement deficits, as well as rigidity, can be accounted for by abnormal processing of the mechanoreceptor sensory input utilized in the generation and execution of movements. The MPTP treated monkey is suggested as a model in which to directly test the hypothesis.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1998

Breadth of base whilst walking: effect of ageing and parkinsonism.

BACKGROUND: The effect of healthy ageing and of parkinsonism on breadth of base whilst walking had not been adequately documented. DESIGN: Height-specific reference ranges for mean foot separation at mid-swing were derived for males and females, age not proving to be a significant influence. METHOD: Normative data were obtained from 164 healthy volunteers, and foot separation in idiopathic parkinsonism (99 patients) was characterized by comparison. RESULTS: Parkinsonism was associated with significantly greater within- and between-subject variability in foot separation. There was a linear trend from increased separation in those with bilateral signs but little functional impairment, to decreased separation in the severely impaired but not yet chair or bed bound. Foot separation was best explained by two clinical signs, rigidity and anatomical postural abnormality. A flexed posture was associated with increased separation, rigidity with decreased, the separation manifested being determined by the net effect. CONCLUSION: In early idiopathic parkinsonism, falling may depend on abnormal posture, and increased breadth of base be compensatory. Later, the decrement in foot separation may become a primary determinant of falls.

Adult↗
PubMed1983

What happened to VIM thalamotomy for Parkinson's disease?

A prospective review of 75 of 190 parkinsonian patients undergoing unilateral thalamotomy was displayed with a computer graphics technique examining three equal consecutive groups from the pre-, early, and late L-dopa eras. Histograms for average function and scattergrams of individual patient's performance preoperatively and up to 2 years postoperatively were prepared. No ipsilateral effects or consistent iatrogenic deterioration of any function were identified. 2 years after surgery, 82% had no tremor in the contralateral fingers or hand and 7% had almost no tremor; contralateral tremor elsewhere was infrequent. Rigidity and manual dexterity improved less strikingly, the latter only reflecting abolition of tremor; locomotion, speech, facial movement and handwriting did not improve. There was no mortality, but 8% had persistent significant complications. VIM thalamotomy remains the treatment of choice for severe drug-resistant parkinsonian tremor.

Adult↗
PubMed2004

Diabetes mellitus and progression of rigidity and gait disturbance in older persons.

BACKGROUND: Parkinsonian-like signs, including rigidity, gait disturbance, and bradykinesia, are common and progressive in old age and are associated with morbidity and mortality. Few risk factors for these signs have been identified. Diabetes mellitus, also a common chronic condition in old age and known to be associated with physical and neurologic disability, may be associated with parkinsonian-like signs. OBJECTIVE: To examine the relation of diabetes to four parkinsonian-like signs. METHODS: Participants were 822 older Catholic clergymen and women who were without clinically diagnosed Parkinson disease or dementia at baseline. For up to 9 years, they had uniform annual evaluations, which included a modified version of the motor portion of the Unified Parkinson's Disease Rating Scale, from which previously established measures of four specific parkinsonian-like signs were derived. Participants were evaluated for the presence of diabetes, based on direct medication inspection and history. RESULTS: Diabetes was present in 128 (15.6%) participants. In random effects models controlling for age, sex, and education, diabetes was associated with worsening rigidity (p < 0.01) and gait (p < 0.05), over an average of 5.6 years of follow-up, but not with change in bradykinesia or tremor. The presence of stroke did not substantially affect the association of diabetes with rigidity but reduced the association of diabetes with gait to a trend (p = 0.08). CONCLUSION: Diabetes may be a previously unrecognized risk factor for progression of parkinsonian-like signs in older persons.

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PubMed2001

Successful management of prolonged gamma-hydroxybutyrate and alcohol withdrawal.

A 27-year-old man was admitted with tremulousness, diaphoresis, tachypnea (28 breaths/min), full-body rigidity, irritability, paranoia, and auditory and visual hallucinations 2 days after stopping long-term gamma-hydroxybutyrate (GHB) and 8 hours after stopping alcohol intake. He received intravenous fluids and tapering dosages of lorazepam to control agitation and rigidity, and recovered with no significant sequelae after 8 days. Abrupt cessation of GHB after high-dosage abuse can precipitate a clinically significant withdrawal syndrome. Lorazepam should be considered for treatment of GHB withdrawal. Concomitant alcohol abuse may mask early GHB withdrawal symptoms and exacerbate withdrawal.

Adult↗
PubMed1990

NMDA antagonists potentiate antiparkinsonian actions of L-dopa in monoamine-depleted rats.

Systemically administered N-methyl-D-aspartate (NMDA) antagonists, MK-801 ((+)5-methyl-10,11-dihydro-5H-dibenzo(a,d)cyclohepten-5,10-imine maleate) and CPP (3-[(+-)-2-carboxypiperazin-4-yl]-propyl-1-phosphonate), potentiate the ability of L-dopa (L-3,4-dihydroxyphenylalanine) to reverse akinesia and to alleviate muscular rigidity in monoamine-depleted rats. On the basis of these findings, it is proposed that NMDA antagonists may be beneficial as adjunctive treatment in the therapy of Parkinson's disease. CPP locally injected into the subthalamic nucleus, entopeduncular nucleus--the rat homologue of the internal pallidal segment--or substantia nigra pars reticulata of monoamine-depleted rats stimulates locomotor activity and alleviates rigidity, whereas local microinjection of CPP into the neostriatum is ineffective. These results make it unlikely that the neostriatum is the site of the antiparkinsonian action of NMDA antagonists in monoamine-depleted rats, whereas the subthalamic nucleus, internal pallidal segment, and substantia nigra pars reticulata appear to be important for the effects of NMDA antagonists.

Animals↗
PubMed1961

Parkinson's syndrome, depression and imipramine. A preliminary report.

Patients with Parkinson's syndrome whose major symptoms are akinesis, rigidity, inertia, depression, irritability and failure of adaptation rather than tremor appear to benefit in a global way from therapy with imipramine. Patients without much over-all functional impairment do not show this improvement. The hypothesis is offered that motivation to move and ability to move are perhaps neurologically as well as psychologically related functions.

Depression↗
PubMed1988

Delayed muscular rigidity and respiratory depression following fentanyl anesthesia.

A delayed effect of fentanyl used for anesthesia may be respiratory distress several hours after surgery. The findings are muscular rigidity, fall in chest wall compliance, hypoventilation, respiratory acidosis, and hypotension. In the past, to our knowledge, this complication was exclusively reported in patients undergoing cardiac surgery, when large fentanyl dosages are employed. This article describes three general surgical patients in whom respiratory distress developed three to five hours following colon surgery when a moderate dose of fentanyl citrate, 55 to 75 micrograms/kg, was used. Initially, all patients had a normal recovery from anesthesia. Later, respiratory distress was successfully treated with a fentanyl antagonist and ventilatory assistance. This delayed toxic phenomenon is thought to be due to the reentry of fentanyl into plasma from deposits in adipose tissue, muscle, and the gastrointestinal tract, leading to a secondary rise in the plasma concentration. It is more likely to be encountered when hypothermia, rewarming, and acidosis are present in the postoperative period. This life-threatening complication is treacherous, since it may occur when the patient has been transferred to the surgical ward and is less closely monitored.

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