Gait ataxia

Ora/-Adverse reactions requiring discontinuation include Pulmonary infiltrates or fibrosis paroxysmal ventricular tachycardia CHF elevation of liver enzymes visual disturbances solar dermatitis blue discoloration of skin hyperthyroidism hypothyroidism. Adverse reactions occurring in at least 3% of patients include CFIF Gl complaints (nausea, vomiting, constipation, anorexia) dermatologic reactions (photosensitivity, solar dermatitis) neurologic problems (malaise, fatigue, tremor/abnormal involuntary movements, lack of coordination, abnormal gait/ataxia, dizziness, paresthesias) abnormal liver function tests. 

Isolated cerebellar infarction withoutinvolvement of the medulla is often difficult to identify, since gait ataxia, vomiting and dizziness may not be accompanied by typical brainstem symptoms (Barth et al. 1994). Cerebellar edema may compress the medulla and the pons leading to conjugate eye deviation to the side opposite the lesion without contralateral hemiparesis. This sign is probably pathognomonic for severe cerebellar mass effect and requires immediate intervention. 

Subacute combined degeneration of the spinal cord is from demyelination of the corticospinal tracts and posterior columns of the spinal cord, leading to gait ataxia and loss of position sense and vibratory sense. Peripheral neuropathy leads to loss of cutaneous sensation and tendon reflexes (Savage and Lindenbaum, 1995). 

A 74-year-old woman had a 3-year history of mild dysarthria, dizziness, and gait ataxia, accompanied by two transient ischemic attacks with involuntary ballistic movements of her left arm lasting several seconds each, and another transient ischemic attack with a right homonymous hemianopia lasting 30 minutes. About 45 minutes after her first-ever oral administration of dipyridamole plus aspirin she developed a transient cerebellar deficit that reproduced features of previous vertebrobasilar ischemic events, as well as severe headache, flushing, and diarrhea. 

Acute cerebellar dysfunction, with gait ataxia, nystagmus, dysmetria, and dysarthria, is the most common form of neurotoxicity (48,49). A rare problem is optic neuropathy and impaired vision (51). 

An unexplained case of permanent neurological deficit, consisting of left facial palsy, right sensorineural hearing loss, gait ataxia, and hemisensory loss in the body and face, has been described after inferior alveolar nerve block (93). 

The oral LD50 for rats is 46 mgkg Convulsions are the principle CNS effect. In birds, acute symptoms include tail feathers spread and pointed either upward or downward, hyperexcitability, jerkiness in gait, ataxia, dyspnea, myasthenia, fluffed feathers, immobility, terminal wing-beat convulsions, or opisthotonos. Mortalities usually occurred 1-9 days following treatment. 

The signs of symptoms of hashish intoxication are lightheadedness, loss of concentration, weakness, palpitations, tremors, postural hypotension, staggering gait (ataxia), and sense of floating. 

Neurological Headache, coma, loss of reflexes, Cheyne-Stokes respiration, seizures, electroencephalogram abnormalities Organophosphate-induced delayed polyneuropathy manifested by flaccidity or paralysis of extremities, paresthesias, footdrop, gait ataxia, spasticity develops 1-2 weeks after exposure Intermediate syndrome 1-4 days after exposure manifested by weakness of proximal limb and respirator muscles, loss of knee reflexes, cranial nerve palsy, death... 

Organophosphate-induced delayed polyneuropathy manifested by flaccidity or paralysis of extremities, paresthesias, footdrop, gait ataxia, spasticity develops 1-2 weeks after expo-... 

A 56-year-old man taking lithium earbonate 400 mg three times daily for a bipolar disorder was admitted to hospital with bronchitis. He was started on levofloxacin 300 mg daily, and within 2 days was noted to have developed gait ataxia, dysarthria, coarse tremor, dizziness, vomiting, and confusion. Lithium toxicity was suspected, and because of the time course of the symptoms, an interaction with levofloxacin was considered responsible. Serum-lithium levels were found to have risen from 0.89 mmol/L (measured 2 weeks previously) to 2.53 mmol/L, and a reduction in his renal function was noted. Both drugs were stopped and the patient recovered over the following 4 days. His lithium level was found to be 1.12 mmol/L at that time. ... 

A 72-year-old woman developed dysarthria, dysmetria, and gait ataxia after taking metronidazole for 3 weeks for an intra-abdominal abscess. The cerebellar syndrome resolved gradually after withdrawal of metronidazole [21 ]. 

Thiamine deficiency is the established cause of Wernicke s encephalopathy (WE), an acute neurological disorder constituting one of two components of Wernicke-Korsakoff syndrome (WKS), a neuropsychiatric disorder characterized by ophthalmoplegia, gait ataxia and confusion/memory loss. Up to 80-90% of these patients with WE go on to develop the more debilitating chronic amnesic state, referred to as Korsakoff s psychosis. 

Nervous system In a retrospective study of the medical records of 707 patients treated with amiodarone over 151 months, there was a cumulative incidence of probable amiodarone-induced neurotoxic effects in 2.8%, 1.6% being referred to a neurology department. The neurological problems included tremor, gait ataxia, peripheral neuropathy, and cognitive impairment. The primary susceptibility factor for amiodarone-related toxicity was duration of treatment, not age, dose, sex, or indication. However, the higher incidence of neurotoxic effects that was observed when amiodarone was first introduced may have been related to a much higher daily dose [32 ]. 

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