Gait disorder

A 46-year-old man chronically abused heroin through inhalation and developed a gait disorder with paresthesia of the legs, incontinence, and impotence. MRI scans showed bilateral subcortical lesions and bilateral signal abnormalities in the corticospinal tract and posterior columns. Motor evoked potentials were slow, with prolonged F wave latency, which is evidence of peripheral nerve disease. Multivitamins and high doses of prednisone did not produce benefit. 

In two patients with Crohn s disease, azathioprine was suspected to have caused severe gait disorders with an inability to walk (41). Within 1 month of treatment, both had joint pains or diffuse arthralgias that were the presumed cause of pseudoparalysis of the legs. In one patient other causes were carefully ruled out and similar symptoms recurred shortly after azathioprine was re-introduced. 

Bellaiche G, Cosnes J, Nouts A, Ley G, Slama JL. Troubles de la marche secondaires a la prise d azathio-prine chez 2 malades ayant une maladie de Crohn. [Gait disorders secondary to azathioprine treatment in 2 patients with Crohn s disease.] Gastroenterol Clin Biol 1999 23(4) 533. ... 

The serum carbamazepine concentration rose from 27 to 76 pmol/l after ritonavir was introduced in a 36-year-old man (89). Dizziness and a gait disorder resolved when carbamazepine was withdrawn. The serum phenytoin concentration was unaffected by ritonavir. 

Animal toxicity is primarily related to ingestion of the plant C. autumnale. Colchicine is available as a pesticide for burrowing animals. The estimated toxic dose for cows is lOgkg with fresh leaves or 2 or 3gkg with dried leaves. Symptoms may include gait disorders, hypersalivation, bloody vomitus, and diarrhea. Death within 72 h has occurred secondary to shock. It is only slightly toxic to cold-blooded and hibernating animals. 

The most effective surgical technique is deep brain stimulation (DBS) of the STN, which decreases outflow from this region (as shown in Fig. 57-2S) and thus reduces input to the thalamus. STN DBS is especially useful for tremor, dyskinesias, gait disorder, and start hesitation. Thalamic DBS and thalamotomy (a focal destructive lesion of the thalamus) can reduce disabling tremor. Pallidotomy (a focal destructive lesion of the GPi) and GPi DBS can help with severe dyskinesias and on/off fluctuations but is not as helpful for bradykinesia. Destructive lesions are immediate and permanent, whereas DBS requires lifelong maintenance. Transplantation of autologous adrenal medulla tissue was unsuccessful, as has been more recent experience in most cases of fetal tissue transplantation. 

The main neurological findings of mental retardation, deafness, gait disorder, spasticity, primitive reflexes and squint are similar to those of DeLong and other investigators (1,2,3,4). These features result in a characteristic neurological syndrome with a wide range of expression from those with minimal disability to those who are totally dependent on others. 

Nervous system An 82-year-old man developed a higher level gait disorder and nocturnal delirium after taking co-trimoxazole (trimethoprim 800 mg -H sulfamethoxazole 160 mg bd) for 37 day 3 days after co-trimoxazole withdrawal his gait returned to normal [184" ]. 

Dakin LE. Probable trimethoprim/sulfa-methoxazole-induced higher-level gait disorder and nocturnal delirium in an elderly man. Ann Pharmacother 2009 43(1) 129-33. 

A deficiency of niacin also affects the nervous system. Numbness is initially observed and later, paralysis, particularly in the extremities is common. Severe cases are characteri2ed by tremor and a spastic or ataxic gait and are frequentiy associated with peripheral neuritis. Left untreated, severe thought disorders can ensue (1). 

Huntington s disease, an autosomal dominant disorder, has a mean age-of-onset of 43-48 years. Symptoms appear gradually and worsen over a period of about 15 years until death occurs. Mood disturbance, impaired memory, and hyperrefiexia are often the first signs, followed by abnormal gait, chorea (loss of motor control), dystonia, dementia, and dysphagia. Cases of juvenile onset (<10 years old) are more severe and most frequently occur when the defective allele is inherited paternaily. About 25% of cases have late onset, slower progression, and milder symptoms. 

Adverse reactions that occurred in 3% or more of patients include the following abnormal gait, abdominal pain, accidental injury, amblyopia, asthenia, ataxia, confusion, cough increased, depression, diarrhea, difficulty with concentration/attention, difficulty with memory, dizziness, ecchymosis, emotional lability, flu syndrome, hostility, infection, insomnia, myalgia, nausea, nervousness, paresthesia, pain (unspecified), pharyngitis, rash, somnolence, speech disorder, tremor, urinary tract infection, vomiting. 

Adverse reactions occurring in at least 3% of pediatric patients include abnormal gait, aggressive reaction, anorexia, ataxia, confusion, constipation, difficulty with concentration/attention, difficulty with memory, dizziness, epistaxis, fatigue, gastroenteritis, hyperkinesia, increased saliva, injury, insomnia, nausea, nervousness, personality disorder (behavior problems), pneumonia, psychomotor slowing, purpura, skin disorder, somnolence, speech disorders/related speech problems, urinary incontinence, viral infection, weight decrease. 

CNS disorders CNS adverse reactions including decreased mental status, gait disturbance, and dizziness have been observed, particularly in patients receiving doses greater than 250 mcg/m /day. Most of these abnormalities were mild and reversible within a few days upon dose reduction or discontinuation of therapy. Exercise caution in patients with seizure disorders and compromised CNS function. Cardiac disease Use with caution in patients with pre-existing cardiac disease, including symptoms of ischemia, CHF, or arrhythmia. 

Angelman syndrome is a devastating neurologic disorder featuring severe mental retardation, a "happy puppet" demeanor, seizures, ataxic gait, and aphasia. 

Very rare disorders include juvenile metachromatic leukodystrophy, adrenoleucodystrophy, Wilson s disease These conditions are associated with movement disorders, particularly gait disturbance. It is important to attempt to distinguish between primary and secondary (antipsychotic related) movement disorders These conditions are characterized by a progressive loss of cognitive skills (in contrast to the more relative decline seen in schizophrenia and other developmental disorders, where a loss of previously learned skill is unusual)... 

After 4 months, he developed numbness and paresis of the legs and hyperalgesia at dermatomes T3 and T4. After 10 months he had marked disturbance of proprioception combined with spinal ataxia and an increasing loss of motor bladder control. There was an intraspinal epidural lipoma in the dorsal part of the spine from Tl-10. The fat was removed surgically and within 4 weeks his gait disturbance and proprioception improved, the sensory deficit abated, and the bladder disorder disappeared completely. 

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