Ralph Greenlee

Amphetamine paired with physical therapy accelerates motor recovery after stroke : further evidence

BACKGROUND AND PURPOSE In animal models of brain injury, administration of numerous pharmaceuticals is reported to facilitate functional recovery. However, only drugs that increase the release of norepinephrine have been shown to promote recovery when administered late (days to weeks) after injury. To determine whether these findings were applicable to humans, we administered the norepinephrine stimulant dextroamphetamine, paired with physical therapy, to hemiplegic stroke patients. METHODS Ten hemiplegic patients who suffered an acute ischemic infarction were entered between days 16 and 30 after onset and randomly assigned to receive either 10 mg of dextroamphetamine or a placebo orally every fourth day for 10 sessions paired with physical therapy. The Fugl-Meyer Motor Scale was used at baseline, within each session, and for 12 months after onset as the dependent measure. Confounding medications such as alpha-adrenergic antagonists or agonists were excluded in all subjects. RESULTS Although there were no differences between the groups at baseline (P = .599), there was a significant (P = .047) difference between the groups when the drug had been discontinued for 1 week and at the 12-month follow-up visit (P = .047). CONCLUSIONS Administration of dextroamphetamine paired with physical therapy increased the rate and extent of motor recovery in a small group of hemiplegic stroke patients. These data support and extend previous findings of the facilitatory aspects of certain types of drugs on recovery from brain injury. The use of neuromodulation may allow the nervous system to adapt previously unused or alternative pathways to relevant external input.

Use of amphetamine in the treatment of aphasia

The effects of d-amphetamine on the recovery of aphasia following stroke was examined in 6 patients. Patients entered the study between 10 and 30 days post onset and were followed for 3 months. The Porch Index of Communicative Ability was used to project a 6 month recovery score. By 3 months post onset, 5 of the 6 patients obtained scores in excess of 100% of the 6 month projections.

MRI evaluation of amyloid myopathy

Amyloid myopathy is a rare complication of primary amyloidosis. The magnetic resonance imaging (MRI) features of two patients with amyloid myopathy were studied. Slight prolongation of muscle T1 and T2 relaxation times was evident but the striking abnormality was marked reticulation of the subcutaneous fat. The clinical findings of indurated extremities far exceeds the minimal signal intensity alteration seen in the muscles. The MR appearance of amyloid myopathy differs from that of other neuromuscular conditions in the minimal changes found in muscle, but the striking abnormality seen in subcutaneous fat makes it distinct from many neuromuscular conditions.

Lower brain-stem origin of the median nerve N18 potential.

A patient undergoing intraoperative median nerve somatosensory evoked potential (MSEP) and brain-stem auditory evoked response (BAER) monitoring showed changes during basilar artery aneurysm clipping. There was loss of the BAER wave V, with preservation of waves I and III. Simultaneously, there also was loss of the MSEP N20 potential, with preservation of the N18, N13 and Erbs point potentials. The patient died and autopsy showed an infarct involving the whole rostro-caudal extent of the pontine tegmentum. This combination of electrophysiologic and pathologic findings may help answer questions regarding the exact generators of different MSEP potentials. In particular, it implies that medullary structures can generate the N18 potential.

Isolated symptomatic peripheral neuropathy in type 1 insulin-dependent diabetes mellitus

Diabetic neuropathy is probably the most frequent of the chronic complications of diabetes, and is usually found in association with diabetic retinopathy and/or nephropathy. We report seven patients with long-standing insulin-dependent diabetes mellitus in whom symptomatic peripheral neuropathy was the first and only documented complication. The diagnosis of peripheral symmetrical neuropathy was based on the presence of symptoms and abnormal physical findings, confirmed with abnormal electrophysiological and/or vibratory and thermal threshold measurements. Diabetic retinopathy and nephropathy were absent. We conclude that in some type 1 insulin-dependent diabetic patients, similar to what has been reported in type 2 non-insulin-dependent diabetes, peripheral neuropathy may be the first chronic complication to become manifest. This observation provides additional evidence to suggest that each of the diabetic complications may have a different pathogenic mechanism.