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PubMed1987

Flunarizine- and cinnarizine-induced extrapyramidal reactions.

Cinnarizine and flunarizine are selective calcium blockers that have been used to treat and prevent vertigo. We studied 15 patients who had extrapyramidal syndromes after taking these drugs. Eleven patients had parkinsonism, one with persistent akathisia as well; one had an orofacial tremor; one, acute akathisia alone; and one an acute dystonic reaction. All but one improved when the drug therapy was discontinued. Seven patients were also depressed during treatment. Cinnarizine and flunarizine must therefore be added to the list of potentially risky drugs known to induce extrapyramidal reactions and depression.

Adult↗
PubMed1993

Local treatment of dystonia and spasticity with injections of botulinum-A toxin.

The use of botulinum-A toxin will be described in two conditions--the extrapyramidal syndrome of dystonia and the pyramidal deficit, spasticity. There is no cure for dystonia and its cause is unknown. Drug therapy is unpredictable and dose-limiting side effects frequently occur with little or no alleviation of symptoms. Spasticity of adductor muscles in the lower limbs causes profound disability and major nursing problems in patients with chronic disorders of the pyramidal tract. As in the case with dystonia, drug therapy is unsatisfactory. At the UBC Movement Disorders Clinic treatment with botulinum-A has been applied to over 400 patients since 1985. The results of the first studies using this treatment in spasmodic torticollis (the most common form of focal dystonia) and spasticity (in late stage multiple sclerosis) will be discussed. As well the effects of long term treatment will be addressed. Botulinum-A toxin is approved treatment for strabismus, blepharospasm and hemifacial spasm. Approval for its use in other focal dystonias is anticipated. The very nature of the agent used for treatment requires that patients be well prepared and reassured before they undergo their first treatment. There is a wide gulf between the patients' preconceived notions about the treatment and reality.

Botulinum Toxins↗
PubMedDate not supplied

Degeneration of the substantia nigra in familial amyotrophic lateral sclerosis.

We have studied a large family with familial amyotrophic lateral sclerosis (FALS) and examined the brain and spinal cord of a 40-year-old male family member at autopsy three years after clinical onset of the disease. The most unusual finding was a severe degree of neuronal loss of the substantia nigra accompanied by gliosis and numerous pigment-laden macrophages. There was marked degeneration of the upper and lower motor neurons and the corticospinal tracts. In addition, there was an unusually severe degree of diffuse degeneration throughout the anterolateral columns of the spinal cord. The posterior columns and Clarke's nucleus were not involved. Nigral degeneration has rarely been reported in FALS. The findings in this case emphasize the great variability of morphologic changes encountered in FALS and raise the question of a relationship between FALS and extrapyramidal disorders such as Parkinson's disease. We conclude that careful postmortem examinations of further cases of FALS are needed to fully define the extent of degenerative changes in this disease.

Adult↗
PubMed1992

Afferent projections to the cholinergic pedunculopontine tegmental nucleus and adjacent midbrain extrapyramidal area in the albino rat. I. Retrograde tracing studies.

The afferent connections of the pedunculopontine tegmental nucleus (PPT) and the adjacent midbrain extrapyramidal area (MEA) were examined by retrograde tracing with wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP). Major afferents to the PPT originate in the periaqueductal gray, central tegmental field, lateral hypothalamic area, dorsal raphe nucleus, superior colliculus, and pontine and medullary reticular fields. Other putative inputs originate in the paraventricular and preoptic hypothalamic nuclei, the zona incerta, nucleus of the solitary tract, central superior raphe nucleus, substantia innominata, posterior hypothalamic area, and thalamic parafascicular nucleus. The major afferent to the medially adjacent MEA originates in the lateral habenula, while other putative afferents include the perifornical and lateral hypothalamic area, periaqueductal gray, superior colliculus, pontine reticular formation, and dorsal raphe nucleus. MEA inputs from basal ganglia nuclei include moderate projections from the substantia nigra pars reticulata, entopeduncular nucleus, and a small projection from the globus pallidus, but not the subthalamic nucleus. Dense anterograde labeling was observed in the substantia nigra pars compacta, entopeduncular nucleus, subthalamic nucleus, globus pallidus, and caudate-putamen only following WGA-HRP injections involving the MEA. The results of this study demonstrate that the PPT and MEA share many potential afferents. Remarkable differences were found that support distinguishing between these two nuclei in future studies regarding the functional organization of the midbrain and pons. The results, for example, confirm our previous observations that the largely reciprocal connections between the midbrain and basal ganglia distinguish the MEA from the PPT. Afferents from the lateral habenula and contralateral superior colliculus represent extensions of more traditional basal ganglion circuitry which further delineate the MEA from the PPT. The results are discussed with respect to the important role of the midbrain and pons in behavioral state control and locomotor mechanisms.

Afferent Pathways↗
PubMed1983

Gerstmann-Sträussler-Scheinker's disease.

Findings are reported in three members of a Japanese family with a chronic familial disease characterized by signs of marked cerebellar dysfunction, mild pyramidal and extrapyramidal dysfunction, and loss or decrease of the knee and ankle jerks. Although the clinical features suggested olivopontocerebellar atrophy, postmortem study of one patient with obvious dementia revealed massive multiform plaques of Kuru type as well as multicentric, senile, and primitive types throughout the central nervous system, most prominent in the cerebellar and cerebral cortices and caudate nucleus. There was degeneration of the spinocerebellar and pyramidal tracts, posterior columns, superior cerebellar peduncles, cerebellar cortex, dentate nucleus, and vestibular nuclei as well as gliosis of the inferior colliculus and cerebellar foliar white matter. There were no cerebral spongiform changes, although slight spongy alteration without glial reaction was present. The clinical and neuropathological characteristics were consistent with those reported as Gerstmann-Sträussler-Scheinker's disease in an Austrian family.

Aged↗
PubMed1994

[Cumulative familial olivopontocerebellar atrophy type IV].

Three affected members of a family with olivopontocerebellar atrophy IV (Schut-Haymaker type) of autosomal dominant inheritance are presented. The five types of olivopontocerebellar atrophy are differentiated on the basis of clinical symptoms and the mode of inheritance. Its clinical symptoms are varied but the cerebellar ataxia of different extent is present in every case which may be followed by pyramidal and extrapyramidal symptoms. Clear differentiation from the other types is based on the destruction of the nuclei of cranial cerebral nerves (IX, X, XII).

Adult↗
PubMed1979

[Diagnosis of subclinical manifestations of the pyramidal syndrome by stimulation electromyography].

The studies were carried out on patients with cerebral and spinal pathology (transient disturbances of cerebral circulation, post-traumatic epilepsy, cervical myelopathy with segmental disorders, etc.). Despite the absence of the clinical manifestations of the pyramid syndrome most patients showed diversely directed shifts of the amplitude of the soleus muscle H-reflex, absence of the depression of this response on high-frequency stimulation, presence of the H-potential in the foot muscles, and an increase of the amplitude of the H-reflex (withdrawn by needle electrodes) of the anterior tibial muscle. It has been concluded that of greater diagnostic value for revealing subclinical forms of the pyramid-extrapyramid insufficiency are electrophysiological findings characterizing the state of the spinal inhibition mechanisms, rather than tests characterizing the level of the motor neuron activity.

Adult↗
PubMedDate not supplied

The neuroleptic malignant syndrome: a missed diagnosis?

The neuroleptic malignant syndrome (NMS) is an idiosyncratic reaction to major tranquilizer drugs characterised by hyperpyrexia, extrapyramidal disorders and altered consciousness. First described in 1968 by Delay and Deniker, early case reports suggested a mortality of between 20 and 30%. Though the syndrome is now more widely recognised, the diversity of its clinical features may not always be appreciated and may lead to diagnostic confusion with other, more common, disorders. We report on two severe cases of NMS: in the first the diagnosis was initially thought to be sepsis from a urinary tract infection, and in the second the primary clinical diagnosis was of a mid brain infarction.

Adult↗
PubMed1993

[A family with Menzel's disease showing dementia and various extrapyramidal symptoms].

UNLABELLED: Recent progress in neurology has revealed that hereditary olivo-ponto-cerebellar atrophy (OPCA) is in fact three different diseases. These are Menzel's disease, in which degeneration in the olivopontocerebellar (OPC) system is quite severe and similar to that of the patient described by Menzel in 1891, spinocerebellar ataxia 1 (SCA 1), in which the gene locus exists in the short arm of chromosome 6, and hereditary OPCA with retinal degeneration. We present a family with Menzel's disease, some of whom showed dementia and various extrapyramidal symptoms including tremor, myoclonus, and choreoathetoid involuntary movement. MATERIALS: This dominant hereditary cerebellar ataxia family had five affected members in four generations. Neuropathological examination of one member (Case 3) revealed Menzel's disease. There was severe degeneration in the OPC system, the substantia nigra, Clarke's column, the posterior column, and the anterior horn of the spinal cord, and slight-to-moderate degeneration in the globus pallidus and subthalamic nucleus. However, the dentate nucleus, spinocerebellar tracts, and oculomotor nucleus including the medial longitudinal fasciculus were spared. The brain weight was 990 g. Case 1 (Case 3's grandmother) developed slowly progressive ataxia at the age of 55. She showed no involuntary movement or dementia. She died at 63 years of age. Case 2 (Case 3's mother) developed ataxia at 42 years of age, followed by tremor of the hands and head, and died at age 57. She did not show dementia. Case 3 (the autopsied case) developed progressive ataxia at 27 years of age, followed by mental deterioration, tremor, myoclonus, and generalized amyotrophy and sensory disturbance during her fifth decade.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

[Abulia: a case of cerebral infarction in the bilateral genua of internal capsules].

A patient was presented with an outstanding symptom of abulia due to cerebral infarcts in the bilateral genua of internal capsules. A 53-year-old woman, generally in good health and active, had no contributory medical history except for hypertension. She was well until August 20, 1988, when she was noted to have become taciturn and absent-minded. In the morning, she got up and went to work as usual. Although she worked without trouble, she hardly talked with her colleagues. After getting home from work, she would lie down without doing any housework, and this was continued on the following day. However, she had no physical problems. She was thus admitted to a hospital on August 22. Lethargy and urinary incontinence were apparent for a few days. Thereafter she became awakeful and could take care of herself. She sat on her bed all the time, and could talk normally with her daughter. She was referred subsequently to the Department of Neurology, Hyogo Prefectural Tsukaguchi Hospital on August 30. On examination, the patient was alert, polite and cooperative with no physical abnormalities except for high blood pressure. Neurological examination indicated the patient to be attentive and well-oriented. Cranial nerves and eye movements were normal except for slight anisocoria and sluggish pupils. There were no muscle weakness, extrapyramidal signs, or cerebellar signs. Deep tendon reflexes were normal. Babinski signs and forced grasping were not noted. A neuropsychological study showed the patient not to be demented, aphasic, or apraxic.(ABSTRACT TRUNCATED AT 250 WORDS)

Akinetic Mutism↗
PubMed2005

Aripiprazole for the treatment of psychosis in patients with Alzheimer's disease: a randomized, placebo-controlled study.

This study compared the efficacy, safety, and tolerability of aripiprazole, a novel antipsychotic, with placebo in patients with psychosis associated with Alzheimer's Disease (AD). This 10-week, double-blind, multicenter study randomized 208 outpatients (mean age, 81.5 years) with AD-associated psychosis to aripiprazole (n = 106) or placebo (n = 102). The initial aripiprazole dose of 2 mg/d was titrated upwards (5, 10, or 15 mg/d) according to efficacy and tolerability. Evaluations included Neuropsychiatric Inventory (NPI) Psychosis subscale and Brief Psychiatric Rating Scale (BPRS), adverse event (AE) reports, extrapyramidal symptoms (EPS) rating scales, and body weight. Overall, 172 patients (83%) completed the study. Mean aripiprazole dose at end point was 10.0 mg/d. The NPI Psychosis subscale score showed improvements in both groups (aripiprazole, -6.55; placebo, -5.52; P = 0.17 at end point). Aripiprazole-treated patients showed significantly greater improvements from baseline in BPRS Psychosis and BPRS Core subscale scores at end point compared with placebo. AEs were generally mild to moderate in severity and included (aripiprazole vs. placebo): urinary tract infection (8% vs. 12%), accidental injury (8% vs. 5%), somnolence (8% vs. 1%), and bronchitis (6% vs. 3%). Somnolence was mild and not associated with falls or accidental injury. There were no significant differences from placebo in EPS scores, or clinically significant ECG abnormalities, vital signs, or weight. In conclusion, aripiprazole showed similar improvements to placebo in psychotic symptoms as assessed by NPI Psychosis subscale scores, but significantly greater effects on BPRS Core and Psychosis assessments in community-living AD patients with psychosis. Aripiprazole was safe and well tolerated in this patient population.

Aged↗
PubMed1997

Pharmacological stimulation of gastrointestinal motility: where we are and where are we going?

Drugs affecting gastrointestinal motility have become valuable in the management of a number of diseases. Medications that enhance the transit of material through the gastrointestinal tract are called prokinetics. Although symptom improvement can be seen in a variety of motility disorders, these medications have not shown a selective benefit for a particular motility disturbance or symptom complex. This class of drugs includes several subclasses, each with a distinct mechanism of action. Amongst the existing prokinetic compounds, dopamine antagonists, on the one hand, and cholinomimetic drugs, on the other hand, should be distinguished. Since compounds endowed with dopamine antagonism have the disadvantage of causing neuroendocrine side effects and/or extrapyramidal dyskinetic reactions (seen especially after metoclopramide), the recently developed non-cholinergic non-antidopaminergic compound, cisapride, seems to be the most effective one. Its main mechanism of action is considered to be the stimulation of myenteric cholinergic nerves with consequent increase of acetylcholine release. Recent evidence suggests that blockade of CCK receptors and stimulation of motilin receptors are also promising avenues to increase gastrointestinal motility. Since drugs acting on 5-HT receptors are presently the best available motor-stimulating compounds, new derivatives are being developed as gastrokinetic drugs. Although the long-acting somatostatin analog, octreotide, and the GnRH agonist, leuprolide, have shown prokinetic properties in particular clinical conditions, their widespread use cannot be recommended at present. Further work is needed to determine the predictive value of objective abnormalities for the efficacy of a drug in the individual patient. This is the crucial point to define a rational strategy in clinical practice, especially to establish if functional investigation is needed before a prokinetic drug be given.

Gastrointestinal Diseases↗
PubMed1989

Pharmacological and anti-emetic properties of ondansetron.

Three main types of 5-HT (serotonin) receptor have been recognised. The 5-HT3 receptor is located on neuronal tissues in the peripheral and central nervous systems. Ondansetron is a highly selective and potent antagonist for this receptor type. The severe nausea and vomiting caused by cytotoxic agents and radiotherapy can be reduced by metoclopramide treatment, but extrapyramidal side effects are common due to antagonism of dopamine receptors. Ondansetron has been found to significantly delay the onset of emesis, and reduce the number of retches and vomits in ferrets receiving cisplatin, cyclophosphamide, or radiation, at much lower doses than metoclopramide and without the associated side effects. Experiments to define the site of action of ondansetron suggest that at least part of its antiemetic action is in the area postrema, though a peripheral site of action in the upper gastrointestinal tract is also a possibility.

Antiemetics↗
PubMed1992

Parenteral ondansetron for the treatment of chemotherapy- and radiation-induced nausea and vomiting.

Ondansetron hydrochloride dihydrate is a 5-hydroxytryptamine (5-HT3) antagonist that was recently approved by the Food and Drug Administration for the treatment of chemotherapy-induced emesis. The mechanism of action is thought to be due to competitive inhibition of specific serotonin receptors in the central nervous system and gastrointestinal tract. In clinical trials with cisplatin-induced emesis, ondansetron resulted in complete control of vomiting (0-2 episodes) in 55-87% of patients during the first 24 hours of chemotherapy administration. It was significantly more effective than metoclopramide in comparative trials. Ondansetron is also being investigated for the treatment of radiation- and anesthesia-associated nausea and vomiting. Studies in animals demonstrate potential efficacy in the treatment of anxiety, drug withdrawal, and schizophrenia. The drug is generally well tolerated, with no reported extrapyramidal reactions.

Antiemetics↗
PubMed1990

Autosomal recessive ataxia, slow eye movements, dementia and extrapyramidal disturbances.

An Arab family with an autosomal recessive form of spinocerebellar degeneration with slow eye movements is reported. Hitherto all the reported cases were either sporadic or of autosomal dominant inheritance. Associated are progressive intellectual impairment and extrapyramidal dysfunction as well as peripheral neuropathy and skeletal abnormalities. Muscle biopsy revealed non-specific mitochondrial abnormalities. The spectrum of eye movement abnormalities is discussed and the literature is reviewed. It is concluded that the hallmark of this syndrome (slow or even absent saccades) is one of a group of oculomotor abnormalities, all being characterized by delayed initiation and slow velocity. The syndrome seems to be related to the olivopontocerebellar degenerations, but differs in that there is in addition selective degeneration of certain tracts and nuclei in the mesencephalon and probably more rostral structures.

Adolescent↗
PubMed1984

Epidermal growth factor immunoreactive material in the central nervous system: location and development.

Epidermal growth factor (EGF) is a potent mitogen with hormonal activity in the gastrointestinal tract. Material cross-reacting with EGF was detected in the central nervous system of the developing and adult albino rat by the indirect immunofluorescence technique. High concentrations of EGF-cross-reacting material were identified in forebrain and midbrain structures of pallidal areas of the brain. These include the globus pallidus, ventral pallidum, entopeduncular nucleus, substantia nigra pars reticulata, and the islands of Calleja . Thus, EGF may represent another gut-brain peptide with potential neurotransmitter-neuromodulator functions in pallidal structures of the extrapyramidal motor systems of the brain.

Animals↗
PubMed1985

Immunohistochemical demonstration of serotonin nerve fibers in the corpus striatum of the rat, cat and monkey.

The distribution of serotonin-containing nerve fibers in the corpus striatum of the rat, cat and monkey was studied with modified peroxidase-antiperoxidase method using serotonin antiserum without any pretreatment. In the neostriatum (caudate nucleus and putamen) of all mammalian species investigated, the immunoreactive fibers were distinct varicose fibers in a fine network. The concentration of these fibers was high in the ventral, medial and caudal neostriatum. Especially in the area bounded by the globus pallidus, serotonin fibers were abundant and compactly arranged along the nucleus. In this area of the monkey, a few thick fibers (tract fibers) were intermingled; they ran along the lateral medullary lamina. Such tract fibers were also observed outside the medial medullary lamina and in the central portion of the medial pallidal segment. The paleostriatum (globus pallidus and entopeduncular nucleus) of the rat and cat as well as the medial pallidal segment of the monkey was diffusely innervated with serotonin fibers composed of numerous varicosities and fine intervaricose segments, while in the lateral pallidal segment of the monkey, the distribution of fibers was scanty and partial. Our results hint at the morphological basis of the serotonergic regulation of the extrapyramidal system in mammals.

Animals↗
PubMed2000

Selection of drugs to treat gastro-oesophageal reflux disease: the role of drug interactions.

Gastro-oesophageal reflux disease is probably the most common acid-peptic disease in Western countries, and the successful treatment of mild to moderate disease with pharmacotherapy has become commonplace. A large number of effective drugs are now available, and so the decision-making process for physicians increasingly relies on considerations other than pure efficacy. Cost, adverse effects and drug interactions have therefore become important, particularly in the most vulnerable patients - children, the elderly and patients who are ill and are taking medications that may influence the efficacy of antireflux therapy. Important drug interactions with antacids include the prevention of the absorption of antibacterials such as tetracycline, azithromycin and quinolones. H2 antagonists, proton pump inhibitors and prokinetic agents undergo metabolism by the cytochrome P450 (CYP) system present in the liver and gastrointestinal tract. Cimetidine is an inhibitor of CYP3A and it may cause significant interactions with drugs of narrow therapeutic range and low bioavailability that are metabolised by these enzymes. The gastroparietal proton pump inhibitors lansoprazole, omeprazole and pantoprazole are all primarily metabolised by a genetically polymorphic enzyme, CYP2C19, that is absent from approximately 3% of Caucasians and 20% of Asians. These drugs may also interact with CYP3A, but to a lesser extent. Interactions with prokinetic agents carry the greatest potential for harm. Metoclopramide is a dopamine antagonist that may cause extrapyramidal effects when administered alone at high concentrations, or when coadministered with antipsychotic agents such as haloperidol or phenothiazines. Cisapride is clearly able to prolong the electrocardiographic QT interval and cause lethal ventricular arrhythmias when its metabolism is slowed by interaction with inhibitors of CYP3A, such as erythromycin, ketoconazole or itraconazole.

Adult↗