Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
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The mute or nearly mute patient who is alert and has good understanding of speech and a right hemiparesis could have Broca's aphasia, akinesia of speech (transcortical motor aphasia), or aphemia. The patient who has Broca's aphasia does not write well, and his speech does not improve greatly with repetition. The speech of a patient with akinesia of speech improves with repetition. The aphemic patient writes normally, but his speech does not improve with repetition. The mute patient whose eyes are open but who is poorly responsive and moves little or not at all could be an akinetic mute (with either a cingulate or a thalamomesencephalic lesion) or have a locked-in syndrome. The latter is diagnosed by asking the patient to look up and down or to open and close his eyes. If he obeys these commands, the physician questions him using a code of eye movement responses. If the patient fails to respond at all, he is an akinetic mute; intense stimulation may result in speech or movement. If the patient is drowsy and has third nerve involvement, the lesion is in the thalamomesencephalic reticular formation. If the patient appears alert and has episodes of agitation, he probably has bilateral lesions in the gyri cinguli. Patients with weakness of the bulbar musculature (facial, palatal, and tongue weakness and dysphonia) may have either upper motor neuron or lower motor neuron lesions. Only bilateral upper motor neuron lesions produce permanent dysarthria. As a typical example, a patient has a transient left hemiparesis with dysarthria and almost completely recovers. Later, however, a right hemiparesis develops and the patient experiences severe bilateral facial weakness, drooling, dysphagia, and severe dysarthria. The absence of atrophy of the bulbar musculature, a hyperactive jaw jerk and gag reflex and, sometimes, inappropriate laughing or crying episodes indicate that the lesion is located above the medulla in the corticobulbar tracts. Flaccid paralysis, absence of the jaw jerk or gag reflex, and absence of other upper motor neuron signs, such as upgoing toes, indicate a lower motor neuron or neuromuscular junction problem. Appropriate tests to rule out myasthenia gravis should be done. The other conditions discussed here are often obvious from their clinical presentation. Although the specific disorder of speech sometimes is helpful in localizing the cause, in most patients, the associated deficits on neurologic examination are of greatest value.
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PMID:Nonlanguage disorders of speech reflect complex neurologic apparatus. 16 83

Antidepressant withdrawal symptoms, following abrupt or gradual discontinuation of antidepressants, include general somatic distress (flu-like syndromes, gastro-intestinal disturbances, myalgias, headache, chills, weakness and rhinorrhea), anxiety, agitation, sleep disturbances, movement disorders, cardiac arrhythmias, delirium and manic reactions. Two cases of delirium, an hypomanic reaction and two general distress and movement disorders are reported. Cases 1 and 2 required admission to a general hospital. The etiology of the delirium was difficult to assess as long as the clinicians did not know that patients were taking antidepressants. Case 3 corresponds to the paradoxical activation following antidepressant interruption. Cases 4 and 5 constitutes light withdrawal syndromes. Most of cases are probably unrecognized. These cases reflect the importance in daily practice of the phenomena. It can be concluded from our study that: antidepressants must not be abruptly discontinued when a somatic disease appears. When a patient treated with a psychotropic drug develops delirium, the withdrawal of antidepressant must be suspected and the prescribing physician contacted to know what kind of psychoactive medication was prescribed.
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PMID:[Withdrawal syndrome from antidepressive drugs. Report of 5 cases]. 129 96

Abrupt or gradual discontinuation of tricyclic antidepressants may precipitate withdrawal symptoms. The most common of these are general somatic or gastrointestinal distress, anxiety and agitation, sleep disturbance, akathisia, parkinsonism, paradoxical behavioral activation and mania. There are very few reports of withdrawal reactions following discontinuation of clomipramine since it has not been in use in the US until recently. 2 patients with withdrawal symptoms following discontinuation of clomipramine are presented. A 45-year-old man had general somatic symptoms, including headache, myalgia, weakness, fatigue (flu-like syndrome) and nervousness and insomnia after clomipramine, 75 mg/d, had been discontinued abruptly. All symptoms disappeared without treatment after 3 days. A 47-year-old woman presented mainly with severe insomnia, anxiety, agitation, jitteriness and tension after discontinuing a low dose of 25 mg/d of clomipramine. Symptoms disappeared after she started self-treatment with 50 mg/d of the drug. It is important to differentiate withdrawal symptoms from relapse of the primary psychiatric disorder.
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PMID:[Withdrawal reactions after clomipramine]. 145 99

The pharmacokinetics of midazolam were investigated following intravenous and intramuscular administration of 0.5 mg of midazolam hydrochloride/kg of body weight to five healthy mixed-breed dogs. One dog also received the same dose of midazolam by oral and rectal routes. The disposition of midazolam following intravenous administration was characterized by very rapid and relatively extensive distribution followed by rapid elimination. Mean (+/- SD) apparent volume of distribution was 3.0 +/- 0.9 l/kg, mean elimination half-life was 77 +/- 18 min, and clearance was 27 +/- 3 ml/kg/min. Following intramuscular administration, absorption was rapid and complete. A mean peak midazolam concentration of 549 +/- 121 ng/ml was reached within 15 min, and systemic availability was over 90% in each dog. Oral administration to one dog resulted in peak midazolam concentrations within 10 min and a systemic availability of 69%. Rectal administration to the same dog yielded very low systemic availability. Midazolam was extensively bound to canine plasma proteins, with the unbound fraction representing less than 4% of the total plasma midazolam concentration. Plasma samples were also assayed for the presence of the major metabolites, 1-OH and 4-OH midazolam. Neither metabolite were detected, probably as a result of rapid elimination of these compounds by hepatic glucuronidation. Behavioral responses to administration of midazolam included initial signs of profound weakness, ataxia and transient agitation followed by a period of quiesence. A normal behavior pattern returned within 2 h of midazolam administration.
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PMID:Pharmacokinetics and preliminary observations of behavioral changes following administration of midazolam to dogs. 148 33

CP-96,345 has been identified as being a highly selective, nonpeptidic agent with subnanomolar affinity for the NK1 receptor. In the present study, we observed that pre but not posttreatment with this agent will produce depression in the second, but not the first phase of the agitation behavior induced by the injection of formalin into a rat's hindpaw. This effect is monotonically dose dependent after intrathecal (10-200 micrograms/10 microliters) or systemic (1-15 mg/kg, ip) administration. Even at the highest dose examined (400 micrograms/10 microliters), there was only a transient motor weakness of the hindpaw. The stereoisomer CP-96,344 has no binding affinity, and has no effect on the formalin response, but shows the same dose profile for motor dysfunction at the highest dose. In contrast, Spantide, a peptidic sP ligand, had only a modest effect upon the formalin response at 1 microgram/10 microliters and produced a prominent, long-lasting motor dysfunction at 4 micrograms/10 microliters. These results provide the first suggestion of sP antagonists having prominent analgesic activity with a significant therapeutic index (analgesic to motor), and emphasizes the probable role of the NK1 class of receptors in the spinal cord in mediating at least one class of nociceptive afferent input.
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PMID:Stereospecific effects of a nonpeptidic NK1 selective antagonist, CP-96,345: antinociception in the absence of motor dysfunction. 172 Nov 2

Hypoglycaemia is possibly the most frequent metabolic emergency, in that insulin-induced hypoglycaemia is a common side-effect of treatment of a common disease. The symptoms are partly sympathetic and related to the release of catecholamines. These symptoms include sweating, tremor, palpitations, sensation of hunger, restlessness and anxiety. Other symptoms are caused by an insufficient supply of glucose to the brain, resulting in neuroglucopenia with symptoms like blurred vision, weakness, slurred speech, vertigo and difficulties in concentration. Symptom recognition is the primary and most effective defence against cerebral dysfunction which is the ultimate consequence of hypoglycaemia. Even in insulin-treated diabetic patients symptom failure might occur. Patients who experience severe episodes of hypoglycaemia do not constitute a special subgroup of patients. However, near-normalization of blood glucose levels have resulted in an increase in the incidence of severe hypoglycaemia. Moreover, the threshold for hormonal counter-regulatory responses in adrenaline, growth hormone and cortisol is lowered after a period of strict metabolic control in insulin-dependent diabetic patients. The glucose level at which the patients become subjectively aware of hypoglycaemia is correspondingly reduced. Other reasons for hypoglycaemia to occur are oral hypoglycaemic agents, especially sulfonylureas which may be potentiated by other drugs. Prolonged hypoglycaemia may be seen after first-order sulfonylureas, and may indicate glucose infusion as treatment. Next to insulin and sulfonylurea, ethanol is the most common cause of hypoglycaemia. In non-diabetics, hypoglycaemia will typically develop 6-24 h after a moderate or heavy intake of ethanol by a person who has had an insufficient intake of food for 1 or 2 days. Insulin-producing tumours, insulinomas and non-islet cell tumours may also be reasons for hypoglycaemia in non-diabetics. Treatment of mild episodes of hypoglycaemia is intake of fast-absorbing carbohydrates. Severe episodes can be treated with either i.v. dextrose or glucagon injected i.m. or i.v. The glycaemic response and recovery of a normal level of consciousness is 1-2 min slower after glucagon than after glucose.
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PMID:Endocrine emergencies. Hypoglycaemia. 173 95

The present paper is part on an extensive follow-up study aimed at the investigation of the effects of in-patient psychotherapy and at the durability of those effects. Using a psychoanalytic oriented personality-inventory (PSKB, Rudolf 1981) 85 phobic patients were examined at the beginning, at the end, and one year after a 6-8 week in-patient psychotherapy. Our results confirmed some of the generally described personality-characteristics in patients with phobia: the phobic symptoms are often accompanied by physical symptoms (sensation of dizziness, weakness sensation, palpitation, sleep disturbance, heavy sweating and breathlessness) and psychic symptoms (anxiousness, depression, restlessness, reduced self-awareness, pedantry, inhibition of aggressive impulses) which could be influenced by psychotherapy. Furthermore we depicted results which have not yet been published in literature.
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PMID:[Personality markers of phobic patients and their change in psychotherapy. Descriptive results of a catamnestic project of the effectiveness of 6-9 week inpatient treatment]. 177 Dec 26

Ceftazidime, a beta-lactamase-stable, third-generation cephalosporin, is widely used for the treatment of serious gram-negative infections. Neurotoxicity has rarely been associated with the drug; however, two of our patients developed ceftazidime-induced neurotoxicity that produced confusion, disorientation, agitation, generalized weakness, and myoclonus. In both patients these symptoms cleared with either discontinuation or reduction of the dosage of ceftazidime. This emphasizes the importance of adjusting the dosage of ceftazidime in patients with renal insufficiency.
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PMID:Neurotoxicity associated with ceftazidime therapy in geriatric patients with renal dysfunction. 192 20

The purpose of this retrospective prediction study was to evaluate potential risk factors for falls in stroke patients in the acute care setting. Charts of 202 stroke patients who experienced falls and 111 stroke patients who did not fall (N = 313) were sampled from two major medical centers in the southwestern United States. Independent variables included: demographics; side of stroke; mental, motor and sensory status; activity level ordered; medications and laboratory values. A 16-variable multiple linear regression risk-factor equation resulted in r2 = .300, a highly predictive finding (F[16,296] = 7.92, p less than .001). Final results indicate that stroke patients with a history of falls, with impaired decision-making ability, that exhibit restlessness, generalized weakness, abnormal hematocrit and are easily fatigued should be identified for surveillance, especially at night when most falls occur.
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PMID:Predictive risk factors associated with stroke patient falls in acute care settings. 214 86

Single oral doses of 10 to 160 mg centpropazine, a new antidepressant (synthesized by CDRI, Lucknow, India) were administered to groups of 4-5 male volunteers, each dose being interspersed with placebo in a double blind, non-crossover study by random distribution. The drug was well tolerated. Drowsiness, heaviness, weakness and/or headache were reported only at doses of 120 mg and above. No adverse effect was noted in various laboratory tests, ECG or vital parameters. In a multiple dose study, volunteers received 40 or 80 mg centpropazine daily for 4 wk. Mild restlessness and insomnia were observed in some subjects receiving 80 mg dose. In this study also no effect was observed in various laboratory tests, ECG or vital parameters.
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PMID:Clinical pharmacological studies on centpropazine--a new antidepressant compound. 262 4


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