Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026837 (muscle rigidity)
 1,077 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of cephalic tetanus presenting with opisthotonus. A 49-year-old man was admitted because of repeated convulsions. The patient was a garbage truck driver known to be alcoholic, who fell down to suffer an injury of the left face two days before the onset of convulsion. Intravenous administration of diazepam and phenytoin partially relieved the convulsions. Anti-tetanus human immuno-globulin was also administered despite absence of typical clinical sign. Six hours later, however, the patient became unable to open the mouth, i.e. lockjaw developed, and the diagnosis of tetanus was made. Additional anti-tetanus human immunoglobulin of 3,000 units and 4,500 units on the next day rapidly relieved the lockjaw, convulsion, and general muscle rigidity without sequalae. The patient showed transient bilateral facial palsy and rotatory nystagmus during the course. Cephalic tetaus is characterized by a history of an injury of the head and a short latency before developing generalized tonic convulsion or opisthotonus. While a typical case presents with lockjaw, our case presented with opisthotonus, presumably because of early systemic lymphatic spreading of tetanus toxin. Early diagnosis and treatment is important to prevent generalized convulsions which are more frequent and sometimes lethal in cephalic tetanus than the common form.
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PMID:[A case of cephalic tetanus presenting with opisthotonus]. 1167 60

Stiff-Person Syndrome (SPS) is an immune-mediated disorder of the central nervous system characterized by muscle rigidity, episodic muscle spasms, and high titers of antibodies against glutamic acid decarboxylase (GAD). The presence of cerebellar ataxia in SPS is extremely rare, but occurs. Clinical observations of ocular motor abnormalities have been noted in a few SPS patients. The purpose of this study is to provide a detailed quantitative documentation of ocular motor abnormalities in a patient with SPS and progressive cerebellar signs. Detailed clinical assessment of a woman with SPS and precise eye movement recordings using the magnetic search coil technique was performed. In addition to other ocular motor abnormalities that included longer latencies for saccades, downbeat nystagmus, and loss of downward smooth pursuit, a rare saccade velocity profile consisting of multi-component saccades was observed. We postulate that these ocular motor findings are related to impairment of GABAergic neurotransmission because antibodies to glutamic acid decarboxylase (GAD-Abs) have been implicated in the pathogenesis of both SPS and some cases of cerebellar ataxia. In addition, this unusual saccadic velocity profile may have important implications for modeling the saccadic system and furthering a complete understanding of saccade generation.
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PMID:A rare saccade velocity profile in Stiff-Person Syndrome with cerebellar degeneration. 1672 26

The history, symptoms, diagnosis and treatment of phencyclidine hydrochloride (PCP) intoxication, the pharmacology of PCP and the detection, identification and analysis of PCP are reviewed. The history of PCP from its synthesis in the early 1950s to the present is discussed. Intoxication with low to moderate doses of PCP resembles an acute, confusing state. High doses may cause serious neurological and cardiovascular complications and the patient is often comatose for several days. Treatment involves supportive psychological and medical measures, and acidification of the urine may further increase PCP clearance. The metabolism of PCP involves primarily hydroxylation followed by conjugation and elimination in the urine. Analysis can be accomplished by a number of instrumental methods, and several commercial test kits based on antigen-antibody interactions are available. PCP's effect on human performance and behaviour is due to its ability to alter the perception of reality in the user. PCP causes a range of effects that include hallucinations, delirium, disorientation, agitation, muscle rigidity, ataxia, nystagmus, seizures, and stupor. PCP has stimulant, depressant, hallucinogenic and analgesic effects. Which of these will be most pronounced is unpredictable and depends on the user's personality, psychological state and the environment of use. The impairment can manifest itself as over-aggressive or reckless driving behavior, or may mimic depressant effects due to PCP's anesthetic and depressant effect.
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PMID:Phencyclidine - Effects on Human Performance and Behavior. 2625 94

Paucity in gamma-amino butyric acid (GABA) due to blockage in the action of glutamic acid decarboxylase (GAD), as seen in the syndrome of anti-GAD antibody, causes adult onset cerebellar ataxia, muscle rigidity, and episodic spasms. Downbeat nystagmus, saccadic dysmetria, impaired ocular pursuit, and impaired cancelation of vestibular ocular reflex are typical ocular motor deficits in patients with syndrome of anti-GAD antibody. We describe opsoclonus, in addition to downbeat nystagmus, in a patient with increased titers of anti-GAD antibody. Paucity in GABA leading to disinhibition to Purkinje target neurons at deep cerebellar and vestibular nuclei might have caused downbeat nystagmus in our patient. Anti-GAD antibody can also increase levels of glutamate the precursor of GABA and the substrate for the action of GAD. We propose that opsoclonus might be due to increased levels of glutamate and subsequent hyperexcitability of excitatory and inhibitory burst neurons leading to reverberation in their reciprocally innervating circuit.
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PMID:Opsoclonus in a patient with increased titers of anti-GAD antibody provides proof for the conductance-based model of saccadic oscillations. 2694 42