Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent papers underline the possible involvement of the central nervous system when an acquired peripheral demyelinating disease occurs and vice-versa. We describe five patients with chronic polyneuropathy and "benign" gammopathy, monoclonal (IgM-K, IgA-k, IgG-k) in three cases and polyclonal (IgG, IgM) in two cases; the monoclonal gammopathies were detected in cases of peripheral nerve disease. Three patients showed tremor and signs of pyramidal system impairment when the peripheral damage had improved or was stable. All cases underwent a longitudinal assessment according to clinical, CSF, EMG-ENG, neuroradiological and pathological criteria. The MRI finding always showed multiple alterations of encephalic white matter. When related to neurophysiological and pathological data supporting a chronic demyelinating neuropathy, such results point to possible encephalic involvement in chronic polyneuropathies due to a pathogenetic mechanism common to both.
 ...
PMID:Evidence of central nervous system involvement in chronic demyelinating neuropathies associated with "benign" gammopathies. 254 77

Infection of cattle with various stocks of Trypanosoma brucei rhodesiense indicated that 49% developed a fatal CNS disease comparable to that found in man. Duration of disease ranged from 85 to 1613 days post infection. All eight stocks of T. b. rhodesiense tested, including those from Ethiopia and Tanzania, induced CNS disease. Blood became positive three to five days after inoculation, and after an initial peak of parasitaemia remained positive for three to five months. Subinoculation of blood into rodents subsequently became negative, although trypanosomes persisted in the lymph nodes for at least 56 to 1613 days. Only animals with CNS disease had detectable parasites in the CSF, usually after the animals had undergone severe deterioration. At post mortem examination trypanosomes could usually be found in the lymph nodes and CSF, and occasionally in the blood. Clinical signs included fever, hyperkinesia, weight loss, cerebellar ataxia, tremor, salivation and hyperaesthesia. A mild to moderate anaemia accompanied a transient thrombocytopenia and leucopenia. Animals subsequently developed leucocytosis. A pleocytosis and elevated total protein in the CSF was found, which persisted in some animals for long periods. Histopathological examination of the brain showed prominent generalized perivascular infiltrates consisting mainly of lymphocytes and plasma cells. Mott's cells were regularly observed. Vascular changes were characterized by swollen endothelium, infiltration of the vascular wall by inflammatory cells, and in some instances perivascular oedema. In the most severe cases evidence of ischaemia consisted of large numbers of astrocytes, rarefaction of the parenchyma, and areas of necrosis with loss of normal architecture. Demyelination was limited to perivascular areas. Occasionally a moderate to severe pancarditis was found.
 ...
PMID:Experimental infection of cattle with Trypanosoma brucei rhodesiense. 261 88

Brain atrophy with mental and neurologic deterioration developing a few months after radiation therapy in patients without residual or recurrent brain tumors has been recognized. Two illustrative case reports of this pathologic entity are presented. Six autopsy cases with this entity including the two cases were reviewed neurologically, radiographically, and histopathologically. All patients presented progressive disturbances of mental status and consciousness, akinesia, and tremor-like involuntary movement. Computerized tomography (CT) demonstrated marked enlargement of the ventricles, moderate widening of the cortical sulci, and a moderately attenuated CT number for the white matter in all six patients. Four of the six patients had CSF drainage (ventriculoperitoneal shunt or continuous lumbar drainage), however, none of them improved. Histologic examination demonstrated swelling and loss of the myelin sheath in the white matter in all patients, and reactive astrocytosis in three of the six patients. Neither prominent neuronal loss in the cerebral cortex or basal ganglia, nor axonal loss in the white matter was generally identified. The blood vessels of the cerebral cortex and white matter were normal. Ependymal layer and the surrounding brain tissue were normal in all patients. These findings suggested that this pathologic condition results from demyelination secondary to direct neurotoxic effect of irradiation. The authors' previous report was reviewed and the differential diagnoses, the risk factors for this pathologic entity, and the indication for radiation therapy in aged patients with a malignant brain tumor are discussed.
 ...
PMID:Subacute brain atrophy after radiation therapy for malignant brain tumor. 270 69

A 64-year-old man was admitted to our department because of muscle cramp, atrophy and weakness of the limbs together with difficulty in walking, which had gradually progressed from age 60. About 1 year prior to admission, he had noticed hand tremor and gynecomastia. On admission, neurological examination revealed diffuse muscle atrophy and weakness of the extremities, which were more obvious on the right side with preponderance in the right leg. Bilateral postural hand tremor was also more prominent on the right hand. Fasciculations were observed both in the extremities and tongue. The remaining cranial nerves and cerebellar functions were intact. Sensation was normal except for slightly decreased vibratory sense in the distal part of the legs. Deep tendon reflexes including jaw jerk were increased with the exception of hyporeflexia of the right leg. Babinski sign was negative bilaterally. Blood examination disclosed slight elevation of CK and fasting glucose level of 110 mg/dl. Glucose tolerance test showed a diabetic pattern. CSF examination showed total protein of 74 mg/dl and IgG of 12 mg/dl. On a series of endocrinological studies, there was no significant elevation of androgen and estrogen both in serum and urine except for slight elevation of serum E1 level. Serum LH and FSH, however, were markedly high, which responded far beyond the normal range following to 0.1 mg injection of LH-RH. These results suggested that gynecomastia might be caused by dysfunction of the hypothalamus-hypophysis system. Brain CT and spine MRI showed no abnormality. Muscle biopsy obtained from the right quadriceps femoris revealed neurogenic abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[A case presenting manifestations of bulbospinal muscular atrophy with senile onset, rapid progression and marked asymmetry]. 275 68

300 patients with sleeping sickness have been admitted, at the AHT clinic of Daloa, over a time period of 22 months. The sex ratio of the patients is 1.5 males for 1 female; the mean age is 25.5 years. The most frequent signs and symptoms observed by clinical examination are: fever (30%), nodes (86.3%), prurigo (43.3%), splenomegaly (15.3%), hepatomegaly (1%), headache (72.6%), vigilance and sleeping disturbances (68.7%), perioral reflexes (67.6%), cheiro-oral reflexes (64.3%), movement disorders consisting of tremor, choreo-athetosis movements, buccal dyskinesia or seizures (35%), motor palsy and gait disorders (15%), tonus disturbances (12.3%), sensitivity abnormalities (17%), endocrine disorders (16.3%), psychiatric symptoms (6.3%). According to CSF status, 261 patients have been classified in second period (P2). This group, although biologically well defined, is in fact a miscellaneous group of clinical signs and symptoms ranging from apparently normal patients to sleeping comatose and cachectic patients. 93% of the patients in this group have peripheral signs associated with neurological symptoms. They are as frequent in the first period as in the second period, with a statistical significance. This is an argument to think that the CNS is early affected in the course of the disease. The classification of the patients in groups of increasing neurological impairments, is in accordance with this hypothesis. 89% of the patients in the second period have only slight neurological signs. This explain how difficult it is for a physician to use melarsoprol in the treatment of all patients classified in second period.
 ...
PMID:[The different present-day clinical picture of human African trypanosomiasis caused by T. b. gambiense. Analysis of 300 cases from a focus in Daloa, Ivory Coast]. 284 37

Four infants suffering from benign non-fluctuating, idiopathic dystonia with onset in the first year are presented. The discussion includes the relationship to childhood-onset dystonia, the significance of the tremor, the neurotransmitters in the CSF, spontaneous recovery, the risk of recurrence and the preference not to intervene orthopaedically.
 ...
PMID:Benign idiopathic dystonia with onset in the first year of life. 287 71

Doxorubicin (DXR) and Mitoxantrone (MXN) were administered into the subarachnoid space of mice or the ventricular system of rats. The maximal non-toxic systemic single dose (zero mortality = LDo) of DXR or MXN was used as reference for planning drug doses for CSF administration. LDo in mice were: 8 mg/kg DXR and 6 mg/kg MXN; in rats: 6 mg/kg DXR and 4.5 mg/kg MXN. Signs of neurotoxicity were remarkably similar in DXR or MXN treatment animals and included: head tremor, atactic-dystonic posture and circling behavior. The toxicity was dose dependent. Doses of greater than or equal to 10% the LDo caused early appearance of clinical signs: a dose of 10% LDo caused neurotoxicity in 90% of DXR treated mice and in only 15% of MXN-treated animals. Treatment with 25% LDo MXN caused neurotoxicity in 30% of treated animals. Doses of less than or equal to 5% the LDo caused a delayed onset of DXR neurotoxicity in one third of treated mice (after 60-90 days). In rats, neurotoxicity was of an early onset and augmented severity following doses of greater than or equal to 5% LDo. Abnormal histopathological findings were detected only in symptomatic animals with early toxicity and were usually restricted to superficial cortical layers in mice or the basal surface of the brainstem in rats. Brains of mice with delayed toxicity were unremarkable. The levels of monoamine neurotransmitters and their metabolites (DA, DOPAC, HVA, NE, 5HT) in the striatum, cortex and cerebellum of mice with early and delayed DXR neurotoxicity did not differ from normal brains.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Early and delayed neurotoxicity of mitoxantrone and doxorubicin following subarachnoid injection. 322 35

Chronic alcoholics who maintain abstinence often demonstrate remarkable improvement of neurological and mental dysfunction. This paper presents an overview of the clinical and laboratory work of our group. Reversible clinical manifestations include psychometric scores, ataxia, tremor, Parkinsonism, dyskinesia, cerebral atrophy, EEG parameters, and a CSF acidosis. Electrophysiological investigations showed that in the in vitro hippocampus of rats fed ethanol for several months there was evidence for diminished long-term potentiation, impaired neuronal inhibitory mechanisms (diminished inhibitory post-synaptic potentials and post-spike after hyperpolarisations), decreased neuronal specific membrane capacitance and increased specific membrane resistance. Golgi stains showed attenuation of hippocampal CA1 neuronal dendrites in rats fed ethanol for five months, which reverted to control size in rats permitted two months of alcohol withdrawal.
 ...
PMID:Reversibility of alcohol-related brain damage: clinical and experimental observations. 347 66

The effects of a wide range of doses of systemically administered cysteamine were studied on locomotor behavior, passive avoidance memory, cortical and cerebrospinal fluid somatostatin-like immunoactivity and cortical levels of dopamine and norepinephrine. High doses of cysteamine (200 and 250 mg/kg s.c.) led to sustained locomotor activation. Doses of 150 mg/kg and above resulted in head and neck tremor and increased defecation. When cysteamine was administered immediately following the acquisition of a passive avoidance response, doses of 50 mg/kg and above resulted in significant attenuation of passive avoidance retention test performance. Cysteamine in doses of 50 mg/kg and above depleted cortical somatostatin-like immunoactivity by approximately 50%. The depletion of cortical somatostatin-like immunoactivity was accompanied by a rapid rise in somatostatin-like immunoactivity in cerebrospinal fluid. In addition to the depletion of somatostatin-like immunoactivity, high doses of cysteamine (150 mg/kg and above) produced changes in cortical levels of norepinephrine and dopamine, reminiscent of dopamine-beta-hydroxylase inhibition. The results of this series of experiments suggest that somatostatin, in addition to its effects on hormonal regulation, may play an important role in behavior and passive avoidance learning and memory. It is possible that the amnesia produced by cysteamine may have been due to the release of somatostatin into CSF from tissue stores, rather than somatostatin depletion per se. It is also possible that the catecholaminergic effects of high doses of cysteamine contribute to the behavioral deficits observed.
 ...
PMID:Cysteamine-induced depletion of central somatostatin-like immunoactivity: effects on behavior, learning, memory and brain neurochemistry. 382 20

A 54-year-old housewife became ill with transient diplopia followed by facial paralysis, tremor of the right hand and a progressively worsening disturbance in gait. Four years after the first appearance of the disease bilateral hypacusia, paralysis of the right hypoglossal nerve, dysarthria, severe spastic tetraparesis with ataxia, urinary retention and an organically induced character change were present. Lumbar puncture fluid contained 51/mm3 lymphocytes and 1164 mg/dl protein. Immunoglobulin A, G and M, synthesised locally, could be detected in cisternal fluid. The serum had a high antibody titre against Ixodes ricinus-Borrelia antigen and the same antibodies, formed locally, were present in the lumbar fluid. The neurological deficiencies improved markedly under parenteral penicillin treatment and the antibody titre decreased. The detection of Borrelian antibodies, especially those synthesised locally in the CSF, enabled an aetiological diagnosis to be made in seven other patients aged 18-47 years in whom the disease had been present for 1 to 8 years. These patients likewise presented symptoms characteristic of a disseminated disease of the CNS, with spastic pareses and evidence in the spinal fluid of chronic inflammation and disruption of CSF barriers in particular. This progressive encephalomyelitis differs from the common and spontaneously healing meningo-polyneuritis (Garin-Bujadoux-Bannworth), the usual manifestation of erythema chronicum migrans of the nervous system, in its progressive nature, its invasion of the CNS and the possible long lasting severe damage when not specifically treated.
 ...
PMID:[Progressive Borrelia encephalomyelitis. Chronic manifestation of erythema chronicum migrans disease of the nervous system]. 400 60


<< Previous 1 2 3 4 5 6 7 8 Next >>