Social future of elderly admitted to acute care hospital: opinion of patient or family as predictive factor of subsequent transfer to long term care.

Acute polyradiculoneuropathy after amitriptyline overdoseDespite extensive use of amitriptyline only five cases of peripheral neuropathies have, to our knowledge, been reported.' 5No polyradiculoneuropathy has so far been related to treatment with amitriptyline. Case reportA 53 year.old depressive woman had been taking' amitriptyline 75 mg and lorazepam 2-5 mg daily in January 1984.At the beginning of February she took soluble amitriptyline 800 mg in a suicide.attempt.She became comatose, with generalised seizures, mydriasis, and urinary retention; her muscle stretch reflexes were normal, blood pressure 90/50 mm Hg, body temperature 370C, and' pulse 100 beats/min.The clinical data and an electrocardiogram were normal.She needed respiratory help and gastric evacuation.The next day she was alert, and respiratory help was stopped.She complained of weakness in her left arm that worsened during the next three days.On examination she had severe flaccid tetraplegia, no muscle stretch reflexes, complete bilateral facial and motor bulbar nerve palsy, and axial muscle palsy, resulting in her being unable to keep her head and trunk upright.Though she complained about tinglinig ensations in her arms and legs and around her mouth, no abnormal sensations could be detected.Her gastrointestinal mobility, bladder function, and postural blood pressures were normal.She required respiratory help again during the next five days.By this time the cerebrospinal fluid, normal five days earlier, had an increased protein concentra- tion (1500 mg/I) with a normal cell count.An electromyogram showed signs of denervation, moderately decreased motor nerve conduction velocities, moderately decreased amplitude ofmuscle potentials, increased distal latencies and F waves, and no sign of a conduction block (table ).The results of tests of liver and renal functions, concentrations of porphyrins, thyroid hormones, and serum vitamins, and for syphilis and diabetes mellitus were normal.She denied having taken any other drugs or suffering from any other symptoms of neuropathy before admission.The cranial nerve palsies disappeared by the beginning of March, the weakness in the arms by the beginning of April, and the weakness in the legs by the beginning ofJune.The cerebrospinal fluid still contained an increased protein concentration (970 mg/i) in March but was normal in June.In August' 1986 investigations showed mild symmetrical w'eakness and amyotrophy in the proximal parts of the arms and legs, resulting in a rolling gait, normal stretch reflexes, and normal sensation.An electromyogram showed the same signs as before (table).