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Symptom motor

Neurologic symptoms Motor weakness has been reported rarely. Most of these cases occurred in the setting of lactic acidosis. The evolution of motor weakness may mimic the clinical presentation of Guillain-Barre syndrome (including respiratory failure). Symptoms may continue or worsen following discontinuation of therapy. Stavudine therapy has been associated with peripheral neuropathy, which can be severe and is dose-related. Peripheral neuropathy has occurred more frequently in patients with advanced HIV disease, a history of neuropathy, or concurrent neurotoxic drug therapy, including didanosine (see Adverse Reactions). [Pg.1858]

Extrapyramidal symptoms, akathisia, dystonia, tardive dyskinesia, drowsiness, headache, dry mouth, orthostatic hypotension Agitation, dizziness, nervousness, akathisia, constipation, fever, weight gain Hypotension, postural hypotension, tardive dyskinesia, photophobia, urticaria, nasal congestion, dry mouth, akathisia, dystonia, pseudo parkin son ism, behavioral changes, headache, photosensitivity Parkinson-like symptoms, motor restlessness, dystonia, oculogyric aisis, tardive dyskinesia, dry mouth, diarrhea, headache, rash, drowsiness... [Pg.295]

The alimentary symptoms may be overshadowed by neuromuscular dysfunction, accompanied by signs of motor weakness that may progress to paralysis of the exterior muscles or the wrist (wrist drop), and less often, of the ankles (foot drop). Encephalopathy, the most serious result of lead poisoning, frequendy occurs in children as a result of pica, ie, ingestion of inorganic lead compounds in paint chips this rarely occurs in adults. Nephropathy has also been associated with chronic lead poisoning (147). The toxic effects of lead may be most pronounced on the developing fetus. Consequendy, women must be particulady cautious of lead exposure (148). The U.S. Center for Disease Control recommends a blood level of less than 10 p.m per 100 mL for children. [Pg.73]

Signs and Symptoms Narcosis Behavioral changes decrease in motor functions ... [Pg.182]

Antipsychotic medications are indicated in the treatment of acute and chronic psychotic disorders. These include schizophrenia, schizoaffective disorder, and manic states occurring as part of a bipolar disorder or schizoaffective disorder. The co-adminstration of antipsychotic medication with antidepressants has also been shown to increase the remission rate of severe depressive episodes that are accompanied by psychotic symptoms. Antipsychotic medications are frequently used in the management of agitation associated with delirium, dementia, and toxic effects of both prescribed medications (e.g. L-dopa used in Parkinson s disease) and illicit dtugs (e.g. cocaine, amphetamines, andPCP). They are also indicated in the management of tics that result from Gilles de la Tourette s syndrome, and widely used to control the motor and behavioural manifestations of Huntington s disease. [Pg.183]

Benign familial neonatal convulsion is an idiopathic form of epilepsy beginning within the first six months after birth. Seizures include generalized and mixed, starting with tonic posture, ocular symptoms, and apnea, and often progress to clonic movements and motor automatisms. [Pg.251]

Episodic ataxia (EA) is an autosomal dominant disorder that brief episodes of ataxia can be triggered by physical or emotional stress. The symptom can occur several times during the day, last for seconds to minutes, and be associated with dysarthria and motor neuron activity, which causes muscle rippling (myokymia) between and during attacks. It is caused by a mutation in a neuronal voltage dependent Ca2+ channel. [Pg.479]

A seizure is an abnormal behavioral (often motoric) activity caused by abnormal electrical activity of the brain. Seizures can be the symptom of a chronic neurological malfunction, i.e. epilepsy, or can appear as single events, e.g. during fever in infants. [Pg.1112]

Tetanus is a disease caused by the release of neurotoxins from the anaerobic, spore-forming rod Clostridium tetani. The clostridial protein, tetanus toxin, possesses a protease activity which selectively degrades the pre-synaptic vesicle protein synaptobrevin, resulting in a block of glycine and y-aminobutyric acid (GABA) release from presynaptic terminals. Consistent with the loss of neurogenic motor inhibition, symptoms of tetanus include muscular rigidity and hyperreflexia. The clinical course is characterized by increased muscle tone and spasms, which first affect the masseter muscle and the muscles of the throat, neck and shoulders. Death occurs by respiratory failure or heart failure. [Pg.1196]

Partial or focal seizures arise from a localized area in the brain and cause specific symptoms. A partial seizure can spread to the entire brain and cause a generalized seizure. Fhrtial seizures include simple seizures in which consciousness is not impaired, jack-sonian seizures (a focal seizure that begins with an uncontrolled stiffening or jerking in one part of the body such as finger, mouth, hand, or foot that may progress to a generalized seizure), and psycho motor seizures. [Pg.253]

The adverse reactions associated widi metoclopramide are usually mild. Higher doses or prolonged administration may produce central nervous system (CNS) symptoms, such as drowsiness, dizziness, Parkinson-like symptoms (tremor, mask-like facial expression, muscle rigidity), depression, facial grimacing, motor restlessness, and involuntary movements of die eyes, face, or limbs. Dexpandienol administration may cause itching, difficulty breadiing, and urticaria... [Pg.472]

Despite the paucity of systematic studies in humans, the available evidence suggests that, like drugs such as alcohol, sedatives, and stimulants, inhalant drugs (i.e., solvents, general anesthetics, and nitrites) exert reinforcing effects and increase motor activity. Furthermore, with continuous use, these drugs appear to induce both tolerance and symptoms of withdrawal. [Pg.280]

Another indication of the importance of DA in motor control is the observation that in humans its precursor levodopa, and DA agonists like bromocriptine, not only overcome the akinesia of Parkinsonism but in excess will actually cause involuntary movements, or dyskinesia (Chapter 14). Also it is well known that DA antagonists like chlorpromazine and haloperidol produce Parkinsonian-like symptoms in humans (and catalepsy in animals) and, as indicated above, reduce the dyskinesia of Huntington s Chorea. Thus DA seems to sit on a knife edge in the control of motor function (Fig. 7.8). [Pg.156]

All such animal procedures suffer from the obvious and basic problem that laboratory animals do not behave like humans and that humans cannot reliably interpret their reactions and behaviour. Thus we know that Parkinson s disease is caused by a degeneration of the dopaminergic nigrostriatal tract but its lesion in animals does not produce any condition which resembles human Parkinsonism, except in primates, even though there are functional tests (e.g. rotational movements) which readily establish that loss of dopamine function and also respond to its augmentation (Chapter 15). By contrast, there are many ways, e.g. electrical stimulation and the administration of certain chemicals, to induce convulsions in animals and a number of effective antiepileptic drugs have been introduced as a result of their ability to control such activity. Indeed there are some tests, as well as animals with varied spontaneous seizures, that are even predictive of particular forms of epilepsy. But then convulsions are a very basic form of activity common to most species and epileptic seizures that are characterised by behavioural rather than motor symptoms are more difficult to reproduce in animals. [Pg.293]

In order to understand how the symptoms of PD could arise from a loss of striatal DA and what can be done to replace it and treat PD, it is necessary to know something of basal ganglia circuitry and the role of DA in it. The scheme to be outlined should, however, be regarded as a working template rather than fully proven fact but there is much evidence for it (Fig. 15.2). Certainly the striatum, i.e. the putamen and caudate nucleus, is accepted as the main receiving area in motor circuits. Information coming to... [Pg.300]


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See also in sourсe #XX -- [ Pg.7 ]




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