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Speech disturbance

Notify the primary health care provider if any of the following occurs pain in the legs or groin area, sharp chest pain or sudden shortness of breatii, lumps in die breast, sudden severe headache, dizziness or fainting, vision or speech disturbances, weakness or numbness in the arms or legp, severe abdominal pain, depression, or yellowing of die skin or eyes. [Pg.556]

In extreme cases of intoxication, a Parkinsonism-like syndrome may result, characterized by speech disturbances, muscle spasticity, tremor, memory loss, mental depression, and marked psychic symptoms permanent disability is likely. Psychosis and suicide are established risks of overexposure to carbon disulfide. ... [Pg.121]

Gilhg P, Sackellares S, Greenberg HS Right hemisphere partial complex seizures mania, hallucinations, and speech disturbances during ictal events. Epilepsia 29 26-29, 1988... [Pg.643]

Demyelination. The role of myelin in the nervous system is to aid in signal transduction. Myelin acts like an electrical insulator by preventing loss of ion current, and intact myelin is critical for the fast saltatory nerve conduction discussed above. Neurotoxicants that target the synthesis or integrity of PNS myelin may cause muscle weakness, poor coordination, and paralysis. In the brain, white matter tracts that connect neurons within and between hemispheres may be destroyed, in a syndrome known as toxic leukoencephalopathy. A multifocal distribution of brain lesions is reflected in mental deterioration, vision loss, speech disturbances, ataxia (inability to coordinate movements), and paralysis. [Pg.287]

Methyl bromide Eye, skin, respiratory tract irritant, GI tract disturbances, CNS effects (tremors) CNS depression, visual and speech disturbances, sensory disturbances, kidney damage... [Pg.540]

A large variation of the duration of the detoxification was noted (Table 1). Only five patients could be treated for less than 10 weeks, while twelve other patients had to be treated for up to 91 weeks. The treatment was discontinued in patients in whom both s-Al and the increment of s-Al after desferrioxamine treatment were below 50 pg/L at two successive occasions). The treatment duration was significantly related to the residual diuresis as all patients with a residual diuresis of a liter/day or more could be treated for less than two months (Fig. 2). Other studies have also established the protective capacity of an even minimal functioning kidney [30, 67]. None of the patients died during treatment with desferrioxamine, and six patients (patient Nos. 11-13, 22, 25, 26) died more than one year after termination of the desferrioxamine treatment, due to causes unrelated to the A1 intoxication. As of November 2001, more than five years after the intoxication episode, 12 of the 17 surviving patients (patient Nos. 11, 12, 14, 16-24) are still alive and none of the patients developed any clinical signs of Al toxicity, like speech disturbances, cognitive defects, bone fractures or dementia-like symptoms. [Pg.13]

Slow, relatively low exposure accumulation of Al over a period of years can lead to a number of clinical manifestations, some of which seem to be bypassed in acute Al encephalopathy due to extremely high exposure to Al. Al encephalopathy is a clinical syndrome and, as can be seen in Table 5, there are similarities and differences in the neurological symptoms of acute and chronic Al encephalopathy. In chronic Al encephalopathy microcytic anemia [41, 93, 95—98] and EEG changes [99-104] can precede clinical symptoms [105]. It is unknown if these symptoms can also precede the clinical symptoms of acute encephalopathy. In contrast to acute Al encephalopathy, where speech disturbances are absent, speech disorders are an important presenting clinical sign of neurotoxicity in chronic Al encephalopathy. The neurological basis of the speech apraxia is obscure but it appears to have elements of dysarthria and dysphasia [33, 73], The initial... [Pg.18]

The outcome of stroke depends on the area of neurones involved and may include weakness or paralysis of muscles, numbness, visual or speech disturbances and coma. [Pg.190]

Gaile S, Noviasky JA. Speech disturbance and marked decrease in function seen in several older patients on olanzapine. J Am Geriatr Soc 1998 46(10) 1330-1. [Pg.325]

The FASTER randomized controlled pilot trial studied the benefit of clopidogrel versus placebo and simvastatin versus placebo initiated within 24-hours of symptom onset in patients with TIA or minor stroke, all of whom were treated with aspirin (Kennedy et al. 2007). The primary outcome was any stroke (ischemic and hemorrhagic) within 90 days. Minor stroke was defined as a score < 3 on the National Institutes of Health Stroke Scale (NIHSS) at the time of randomization and TIA was defined in the usual way. In addition, patients were excluded if they did not have weakness or speech disturbance or if symptom duration was less than five minutes. [Pg.246]

Neurologic Headache, ptosis of eyelid, focal facial paralysis, speech disturbance... [Pg.32]

No fatalities have been reported in monotherapy convuisions, sedation, speech disturbance, biurred or doubie vision, metaboiic acidosis, impaired coordination, hypotension, abdominai pain, agitation, dizziness... [Pg.466]

All the above syaptoas aarked speech disturbed difficulty in swalloving restlessness and fatigue headache dey, hot skin difficulty in alcturleion reduced Inteatlnal peristalsis... [Pg.82]

Since 1976, aluminium has been known to be a cause of encephalopathy, a potentially fatal condition occurring primarily in patients on chronic dialysis (21). Difficulties in speech, disturbances of consciousness, and ataxia can be followed by psychotic episodes, personahty changes, myoclonic jerks, electroencephalographic abnormalities, convulsions, and dementia. Accumulation of aluminium can be demonstrated in the gray matter of the brain and in other tissues. If not too advanced, the condition can recede after reduction of aluminium intake and use of deferoxamine. [Pg.98]

Typical symptoms of lithium intoxication are summarized in Table 2 [122-127]. The clinical picture of hthium intoxication is dominated by neuromuscular and cerebral symptoms in mild cases apathy, muscle weakness, tremor, and unsteady gait are seen. In more severe cases speech disturbances, myoclonic twitching, coma and convulsion can occur. Pulse irregularities and circulatory collapse may supervene. Lithium often causes T-wave flattening or inversion on the electrocardiogram, but clinically important cardiovascular effects are rare, with sinus-node dysfunction reported most often [123]. Residual neurological sequelae consisting of cerebellar dysfunction with ataxia, neuropathy and supra-bulbar symptoms are not unusual. [Pg.741]


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See also in sourсe #XX -- [ Pg.45 ]




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