Unilateral abolition of extrapyramidal rigidity after ipsilateral cerebellar infarction.
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Aged↗
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Results for “EXTRAPYRAMIDAL TRACTS”
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Gastrointestinal symptoms in Parkinson disease: 18-month follow-up study.
In a recent study we identified abnormal salivation, dysphagia, nausea, constipation, and defecatory dysfunction as those gastrointestinal (GI) symptoms associated with Parkinson disease (PD) and characterized their relationship to PD severity and therapy. In this study, we re-evaluated these symptoms and their relationship to parameters of PD 18 months later. Sixty-six percent of the original participants responded. Over the 18 months, 68% of originally untreated PD subjects commenced anti-PD therapy. Abnormal salivation, dysphagia, nausea, constipation, and defecatory dysfunction were again identified as those GI symptoms more common in PD. Constipation increased both in severity and frequency. Comparison of GI symptom scores and parameters of PD dysfunction failed to reveal significant progression of either GI symptomatology or PD dysfunction, or the development of new GI symptoms over the 18-month period. This study validates our GI dysfunction assessment system and confirms abnormal salivation, dysphagia, nausea, constipation, and defecatory function as those GI symptoms truly associated with PD. A direct relationship between PD and its related GI symptoms is again supported.
Aged↗
Dentatorubral-pallidoluysian atrophy. Clinical features of a five-generation Danish family.
We describe the first Danish family with dentatorubral-pallidoluysian atrophy (DRPLA), containing 16 clinically affected individuals in five generations. Inheritance is autosomal dominant. The disorder was diagnosed as Huntington's disease (HD), but analysis of the IT15 gene for HD revealed normal alleles. The diagnosis of DRPLA was based on the finding of elongated CAG repeats in the B37 gene on chromosome 12 in affected individuals. The age at onset ranged from 13 to 60 years, with the most severe clinical picture being associated with onset in childhood. Clinical features included varying combinations of dementia, euphoria, visuomotor disturbances, speech problems, ataxia, tremor, epilepsy and involuntary movements presenting as chorea, athetosis, and dystonia. We discuss characteristics of DRPLA that may enable the differentiation from HD on a clinical basis. In conclusion, DRPLA should be considered and DNA analysis is recommended in patients manifesting varying combinations of extrapyramidal and cerebellar symptoms, especially when clinical features show pronounced intrafamilial variability, and dyscoordination, tremor, myoclonus, epilepsy, and euphoria are part of the syndrome.
Adult↗
Hashimoto's myoclonic encephalopathy: an underdiagnosed treatable condition?
We report two patients with subacute diffuse encephalopathy characterized by confusion, myoclonic encephalopathy, and mild akineto-rigid extrapyramidal signs in one case and by apathy, memory deficit, and partial complex seizures in the other. Hashimoto's thyroiditis with high titers of anti-thyroglobulin antibodies was diagnosed in both patients, who were unresponsive to anticonvulsant medication, but showed rapid neurological improvement following steroid treatment. On neuropsychological examination, predominant frontotemporal dysfunction was noted. Electroencephalographic activity was remarkable for its rhythmical delta activity, unresponsive to, or even paradoxically increased by, anticonvulsant treatment. On magnetic resonance imaging, atrophy with temporal predominance was found. These observations support the idea that this potentially treatable dementia and movement disorder should be classified as a separate clinical entity.
Adult↗
Raynaud's phenomenon in a case of multiple system atrophy.
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Autonomic Nervous System↗
Features resembling Tourette's syndrome in developmental stutterers.
Developmental stuttering (DS) may be related to the extrapyramidal motor system and shares many clinical similarities with Tourette's syndrome (TS), which is widely believed to be associated with extrapyramidal dysfunction. Twenty-two stutterers were examined for neuropsychiatric features commonly seen in TS, including tics, obsessive-compulsive behaviors (OCB), and attention deficit disorders. Eleven stutterers displayed motor tics, and symptoms of OCB were observed at rates similar to those seen in persons with TS. Few stutterers demonstrated significant attentional deficits. Findings are consistent with models suggesting extrapyramidal involvement in DS and raise the possibility that DS and TS are pathogenetically related.
Adolescent↗
Pharmacopsychiatry and iatrogenic Parkinsonism.
Through the study of the pharmacological and clinical actions of chlozapine, a new drug used in psychiatry, we are questioning one of the traditional statements on the therapeutic action of antipsychotics: the affirmation that those must have, concomitantly, antipsychotic action and intense extrapyramidal effects (drug-induced parkinsonism). Combining our own investigations and those of other authors, the generally accepted concepts on the possible biochemical mechanisms involved in the etiology of endogenous psychosis are criticized. Although there is evidence of alterations of the dopaminergic system in schizophrenia and also changes due to the action of neuroleptics, we cannot reject, given the dissociation of effects obtained with chlozapine, the possibility that the repercussion on the nigrostriatal dopaminergic system be only one of the many probably mechanisms of action of psychotropic drugs. Thus, such anatomical and neurochemical systems could be involved only in a secondary manner in the biochemical alterations typical of schizophrenia.
Brain↗
The Parkinsonian syndrome and its dopamine correlates.
The urinary excretion of free dopamine in 37 untreated parkinsonian patients correlated negatively with the severity of rigidity and akinesia (p less than 0.025) and with total neurologic deficit (p less than 0.05). In a parallel study of psychiatric patients, those with the lowest levels of urinary free dopamine before treatment were the most vulnerable to, and developed the most severe, secondary parkinsonian rigidity (p less than 0.005), akinesia (p less than 0.05), and total deficit (p less than 0.01) when they were subsequently treated for two weeks with trifluoperazine. In neither study was there a significant correlation between free urinary dopamine and tremor. These studies directly associate the level of free dopamine in the urine with the severity of the parkinsonian syndrome. Therefore, although many peripheral sources contribute to urinary free dopamine, a small decrease in the level may actually reflect the severity of the disturbance of central dopamine metabolism and the known deficiency of dopamine in the neurons of the parkinsonian brain.
3,4-Dihydroxyphenylacetic Acid↗
Failure of L-dopa to relieve activated rigidity in Parkinson's disease.
Rigidity in Parkinson patients can be easily quantitated by determining net work required to passively flex and extend the forearm through an arc of 100 degrees. Rigidity thus measured can be subdivided into two very distinct types, resting and activated. Resting rigidity, measured while the patient is relaxed, responds to all effective therapeutic agents and correlates closely to degree of clinical improvement. Activated rigidity, measured during voluntary activity, is not relieved by any presently available medical treatment. It remains unchanged at pre-therapy levels even in patients who may temporarily appear to have dramatic improvement in clinical symptomatology. Longitudinal measurements made in hundreds of parkinson patients over intervals ranging from 5 to 15 years show continuing high levels of activated rigidity through the entire period of study. In marked contrast to our wide experience with parkinson patients is a single, well documented case of Wilson's disease who appears to have recovered completely both by clinical examination and by all of our machine measurements. This patient had high levels of extrapyramidal deficit, repeatedly measured over a period of four months when penicillamine therapy was being investigated. He then suddenly reverted to normal and returned to full time employment. High values of resting rigidity activated rigidity, akinesia and resting tremor all reverted to normal and have remained normal for the past 6 years. The implication of this study is that L-dopa and related treatments only mask the symptomatology of Parkinson's disease and are not retarding the underlying pathological process. Penicillamine, on the other hand, probably does relieve the destructive process in Wilson's disease and may in early cases, permanently relieve the extrapyramidal dysfunction.
Adult↗
Agents acting on central dopamine receptors.
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2-Naphthylamine↗
Age-related changes in local glucose utilization in the brain.
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Aging↗
The depolarization block hypothesis of neuroleptic action: implications for the etiology and treatment of schizophrenia.
Antipsychotic drugs are known to block dopamine receptors soon after their administration, resulting in an increase in dopamine neuron firing and dopamine turnover. Nonetheless, antipsychotic drugs must be administered repeatedly to schizophrenics before therapeutic benefits are produced. Recordings from dopamine neurons in rats have revealed that chronic antipsychotic drug treatment results in the time-dependent inactivation of dopamine neuron firing via over-excitation, or depolarization block. Furthermore, the clinical profile of the response to antipsychotic drugs appears to correspond to the dopamine system affected: antipsychotic drugs that exert therapeutic actions in schizophrenics inactivate dopamine neuron firing in the limbic-related ventral tegmental area, whereas drugs that precipitate extrapyramidal side effects cause depolarization block of the motor-related substantia nigra dopamine cells. One factor that remains unresolved with regard to the actions of antipsychotic drugs is the relationship between dopamine turnover and depolarization block--i.e., why does a significant level of dopamine release or turnover remain after antipsychotic drug treatment if dopamine cells are no longer firing? We addressed this question using an acute model of neuroleptic-induced depolarization block. In this model, dopamine cells recorded in rats one month after partial dopamine lesions could be driven into depolarization block by the acute administration of moderate doses of haloperidol. However, similar doses of haloperidol, which were effective at increasing dopamine levels in the striatum of intact rats, failed to change dopamine levels in lesioned rats. This is consistent with a model in which neuroleptic drugs exert their therapeutic effects in schizophrenics by causing depolarization block in DA cells, thereby preventing further activation of dopamine neuron firing in response to external stimuli. Thus, attenuating the responsivity of the dopamine system to stimuli may be more relevant to the therapeutic actions of antipsychotic drugs than receptor blockade or decreases in absolute levels of dopamine, which could presumably be circumvented by homeostatic adaptations in this highly plastic system.
Antipsychotic Agents↗
Effects from the sensorimotor cortex on the spinal cord in cats with transected pyramids.
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Animals↗
The differential effects of baclofen on segmental and descending excitation of spinal interneurones in the cat.
Intravenous baclofen (1-6.25 mg kg-1) substantially reduced the monosynaptic excitation of neurones in the intermediate nucleus of the cat spinal cord by impulses in group I extensor muscle primary afferent fibres, but had little or no effect on excitation by stimulating fibres of the ipsilateral dorsolateral funiculus or the contralateral red nucleus. Relatively low concentrations of baclofen thus appear not to influence the release of excitatory transmitter from the terminals of rubrospinal, corticospinal and long descending propriospinal fibres, in contrast to the reduction of the release of primary afferent transmitters.
Animals↗
Afterhyperpolarization in neurones of the red nucleus.
Afterhyperpolarization (AHP) following single or short trains of spikes in rubrospinal neurones (RN neurones) of the cat has been studied with intracellular recording techniques. The AHP amplitude was potential dependent; it increased with depolarization and decreased with hyperpolarization and had an extrapolated reversal potential about 20 mV below resting membrane potential. The AHP was associated with an increase in the membrane conductance and it was concluded that the AHP is primarily caused by an increase in membrane conductance to potassium ions. The time course of the conductance change underlying the AHP was measured with short current pulses and calculated from the AHP voltage. The AHP following a single spike was conditioned at different interspike intervals by a preceding spike (or several spikes). In many RN neurones the AHP (conductance) following a spike added approximately linear to that generated by a preceding spike. In most cells, however, the AHP following a spike was instead depressed by a preceding spike. The summation of AHPs increased progressively, while the depression appeared to be already maximal with one preceding spike. The depression was then approximately constant for interspike intervals less than the AHP duration. It will be shown in a following paper that these properties of the AHP are reflected in the behaviour of the repetitive discharge evoked by constant current pulses in the same neurones.
Action Potentials↗
Differential effects of stimulation of the cat's red nucleus on lumbar alpha motoneurones and their Renshaw cells.
The red nucleus region was stereotaxically stimulated with short trains of high-frequency alternating current pulses in anaesthetized cats. The effects were studied, in contralateral lumbar segments, on the responses of microrecorded individual Renshaw cells (RCs) to antidromic or orthodromic test shocks of ventral root or muscle nerve fibres. Monosynaptic reflexes (MRs) of their motoneurone pools were recorded from one of the cut lumbar ventral roots. Averages of 10-20 replicate test responses of the RC (converted into instantaneous frequency curves, IFCs) and of the MR shapes were computed and graphically displayed. 2. Orthodromic (afferent) test shocks induced simultaneously MRs as well as responses of a RC belonging to the same motor pool. From their paired records at systematically varied shock strengths, whole "linkage characteristics" of the relation between the two events could be obtained, representing the functional linkage from the motoraxon collaterals to the RC under study. The overall result of rubral conditioning was a change in the course of the characteristic, which indicated a reduction of this linkage (= relative inhibition of the RC against its recurrent input). 3. Sequential trials with test shocks of constant, submaximal strength were performed with 45 individual RCs. The clearest results were obtained with RC responses to antidromic ventral root shocks: 65% of the RCs were partially inhibited by rubral conditioning. Interposed minor facilitory subcomponents could be seen in the course of inhibited IFCs. Mixed sequences of manifest inhibitory/facilitory effects were observed in 11%; reversed sequences (facilitory/inhibitory) did not occur. A pure but weak facilitation was found in only one case, paralleled by an increase of the MR. RCs belonging to either extensor or flexor motor pools were affected about equally. A little over 20% of the tested RCs remained uninfluenced by rubral stimulation. 4. The MRs, induced by constant, submaximal, orthodromic test shocks, were usually enhanced with only few exceptions, by rubral stimulation. The effects on the orthodromic RC responses were mainly inhibitory, but could be more or less masked by the concurrent increase of the MR, providing a stronger recurrent input to the RC. Such inhibition could be uncovered, however, by observing the above described linkage change. 5. Variation of several parameters of rubral conditioning (train duration, timing of train with respect to test shock, strength of train) modified the inhibitory effects on antidromic RC responses to a certain extent without changing their principal character.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
The distribution and origin of the ipsilateral descending limb of the brachium conjunctivum. An autoradiographic and horseradish peroxidase study in the rat.
The distribution, organization and origin of the ipsilateral descending limb of the Brachium Conjunctivum (B.C.), have been studied in the rat by using anterograde and retrograde tracing techniques. After injections of tritiated leucine/proline into the lateral cerebellar nucleus, covering both its medial part, corresponding to the dorsolateral hump (DLH) of Goodman et al. (1963) and its lateral part, (designated here as the lateral dentate, LD), and the neighboring interposed nucleus (NI), emerging fibres are numerous and leave laterally from the B.C. On the contrary, injections restricted to LD reveal very few such fibers. Within the lateral parvocellular reticular formation (LPRF) terminal labelling is heavy, and moderate to sparse within the adjacent trigeminal complex. Rostro-caudally, silver grain accumulation within the LPRF extends from the level of the motor trigeminal nucleus (VM) to the pyramidal decussation, exhibiting a cephalocaudal decrease of grain density. Within the trigeminal complex, labelling occurs in the caudal VM, the dorsal portion of the principal sensory nucleus, and within and around the trigeminal spinalis oralis. In addition, the area surrounding the VM (in part corresponding to the supratrigeminal region of Lorente de Nó 1922, 1933) is moderately labelled. After injections of HRP into various levels of the ipsilateral descending B.C.'s projection field, retrogradely labelled cells are numerous within the DLH. A slightly lesser amount of labelled cells are found in the lateral half of the NI, primarily concerning the nucleus interpositus posterior. Within the LD, only a few labelled cells are observed: these are mainly restricted to the dorsal portion at rostral levels of the nucleus. The results obtained by both the anterograde and retrograde studies suggest an absence of a topographic organization within this descending B.C. component. The possible functional meaning of these results is discussed.
Animals↗
Cerebral cortical areas of origin of excitation and inhibition of rubrospinal cells in the cat.
The relations between the cerebral cortex and the red nucleus have been studied in acute, chloralose anaesthetized cats using intracellular recording techniques. Stimulation of the cerebral cortex induces in rubrospinal cells a short latency excitation followed by a long lasting silent period. The evidence is presented that at least a great part of the latter is due to genuine IPSP evoked in these cells. Three populations of rubrospinal neurones have been distinguished according to the cortical origin of their afferents: one group receives projections from the forelimb cortical area. These cells project to the cervical spinal cord and thus should control the forelimb. The second group receives projections from the hindlimb cortical area. These cells project to the lumbar spinal cord and should control the hindlimb. The third group of rubrospinal neurones receives convergent projections from both forelimb and hindlimb cortical areas. If these cells have collateralized axons terminating in both rostral and caudal spinal cord, they could contribute to the coordination of fore- and hindlimb movements. The projections originate in cytoarchitectonic areas 1-5 i.e. in the primary motor and sensory areas and in the rostral portion of the parietal area. No projection has been found from area 6 (premotor) or from area 7 (caudal parietal). The projection upon single rubrospinal cells has been found to originate from large cortical regions with a large overlap between those with excitatory and inhibitory actions. This could indicate the intermingling of cortical cells transmitting both effects.
Animals↗