The sword of Damocles: the psychosocial impact of familial spinocerebellar ataxia in South Africa

It has been recently recognized that increased titers of serum anti-GM1 antibodies may be associated with motoneurone diseases or with multiple motor neuropathy with or without conduction block and also with chronic sensorimotor neuropathy and Guillain-Barré syndrome. Santoro et al. were the first to note that anti-GM1 antibodies were able to bind to the nodes of Ranvier of the sural nerve of a patient with clinical signs and symptoms mostly resembling amyotrophic lateral sclerosis who also showed, in nerve conduction studies, multifocal motor nerve fibers conduction block and serum IGM anti-GM1 antibodies. The two patients presented in this report had asymetrical motor neurone disease with signs and symptoms of lower motoneurone involvement, and other signs, in the first patient, which suggested the existence of upper motoneurone damage. Besides, the second patient also had clinical sensory impairment in the lower limbs. Electrophysiologically, none of them had nerve conduction block but both showed inexcitable median and sural nerve sensory fibers. Both had high titers of anti-GM1. A sural biopsy of both patients showed immunoglobulins into the sensory fibers. However, we do not know whether the anti-GM1 antibodies bind to a cross-reactive glycolipid other than the GM1 itself. In any case, it seems that the presence of anti-GM1 antibodies might be a marker signalling a potentially treatable immune disorder which may have signs of lower and upper motor neurone disease and, also, clinical and electrophysiological evidences of peripheral sensory involvement.     

Intravenous immunoglobulin treatment in paraneoplastic neurological syndromes with antineuronal autoantibodies

OBJECTIVE: To evaluate the effect of intravenous high dose human immunoglobulin (IVIg) therapy on the clinical course and autoantibody titres of patients with neurological paraneoplastic syndromes. METHODS: Twenty two patients with paraneoplastic encephalomyelitis and sensory neuronopathy syndrome associated with anti-Hu antibodies (18) or paraneoplastic cerebellar degeneration (PCD) with anti-Yo antibodies (four), were treated with 1-26 (mean 5.8) cycles of IVIg. The Rankin scale was used to evaluate the response. RESULTS: The only serious toxicity was one case of haemolytic anaemia. Twenty one patients were evaluable for therapeutic response. One patient, with subacute sensory neuronopathy (SSN), improved for at least 15 months, 10 remained stable (eight with anti-Hu and two with anti-Yo antibodies), and 10 deteriorated (eight with anti-Hu and two with anti-Yo antibodies). In seven of the 10 patients who stabilised, the syndrome had already made a plateau when the treatment was started but three patients (one with anti-Hu and two with anti-Yo antibodies) who had still been progressing stabilised for six, eight, and more than 48 months, including one patient with SSN who achieved stabilisation when the neurological dysfunction was only moderate (Rankin scale = 3). Another patient with SSN and initial stable response worsened when IVIg was reduced and improved when it was increased. No significant predictive factors of outcome could be identified but improvement or stabilisation was more frequent in patients with isolated involvement of the peripheral nervous system (62%) than in patients with evidence of CNS damage (37%) at the onset of treatment. Stabilisation in patients with CNS involvement was only achieved when the neurological dysfunction was already severe (Rankin scale > 3). The titres of autoantibodies did not change significantly. CONCLUSION: Treatment with IVIg at the doses given in the present protocol was not effective in paraneoplastic CNS syndromes associated with antineuronal antibodies. The role of this regime in the treatment of SSN should be further evaluated.     

Abnormal sensory nerve conduction in multifocal demyelinating neuropathy with persistent conduction block

Two patients exhibited chronic, slightly asymmetric weakness and wasting with fasciculations of the upper limb and hand muscles. Motor nerve conduction studies showed features of multifocal conduction block in nerve segments other than those usually involved in entrapment syndromes. The F wave was markedly delayed in the median and ulnar nerves. Transcranial cortical and cervical root magnetic stimulation showed bilaterally delayed thenar responses with normal central conduction time. Needle electromyography demonstrated a chronic denervation pattern with large polyphasic motor units in several muscles of the upper limbs. Sensory symptoms were mild and limited to paresthesias in the fingertips. Sensory nerve conduction velocity and sensory nerve action potential amplitudes were normal in elbow-to-wrist and wrist-to-finger segments of the median and ulnar nerves, but there was a delayed cortical response and unrecognizable Erb's point and cervical responses in the somatosensory evoked potentials to median nerve electrical stimulation. Electrophysiologic examination was normal in most nerves of the lower limbs. These two patients, meeting clinical and electrophysiologic criteria of multifocal neuropathy with conduction block, demonstrate that sensory fibers may also be involved in this syndrome.     

Peripheral motor and sensory nerve conduction studies in haemodialysis patients. A study of 54 patients

Peripheral motor and sensory nerve conduction velocities were studied prospectively in 54 chronic haemodialysis patients. The most sensitive parameters for the detection of polyneuropathy were the deep peroneal nerve motor conduction velocity, the sural nerve sensory conduction velocity and the H-reflex latency and H-index of the S1 roots. All patients examined were found to present at least one abnormal nerve conduction parameter. In the present study the side of the arteriovenous shunt had no statistically significant effect on the sensory and motor nerve conduction velocities in the upper extremities. There was a significant correlation between H-reflex latency and H-reflex index, and between H-reflex latency and sural nerve sensory conduction velocity.     

Multifocal motor neuropathies with conduction blocks. 39 cases

Clinical, biological and electrophysiological features from a cohort of 39 multifocal motor neuropathies with conduction blocks (NMM with CB) have been studied. There were 29 males and 10 females with an average of 47.3. At the first evaluation, the mean duration of the symptoms was of 8 years with extremes between 1 and 28. Pain and paresthesias were present in respectively 10 and 18 p. 100 of the patients. Fasciculations and cramps were observed in more than 2/3 of the cases. Three patients had tremor at rest. Upper limb muscular weakness was the predominant initial symptom (84.6 p. 100). The weakness always affected distal and unilateral muscles. Radial and cubital nerve distribution are mainly affected and in half of the cases an unilateral motor deficit in the lower limb was associated. Muscle atrophy was frequent (74 p. 100) and rapidly developed in the first 2 years. Reflexes were decreased or absent in 64 p. 100. In 78 p. 100 of cases, biological study showed normal serum immunoelectrophoresis and CSF. IgM anti-GM1 antibodies were found in 24/36 patients. Very high titres were found in 5 cases. All patients had CB in upper limbs. The preferential localizations of the CB were equally at the median and ulnar nerves. Only 7 patients had CB localized to the lower limbs. In many cases, marked reduction of the motor amplitude prevented the detection of CB, marked reduction of the motor amplitude prevented the detection of CB. Moderate fibrillation potentials were found in 28 p. 100 of patients. Giant muscular unit potentials were frequent (21/39). F-waves in nerve with CB were always abnormal with marked increased latencies. Late responses sometimes seemed to be repeater F-waves. Axon reflexes were detected in 5 cases. The late responses abnormalities could precede the block. Clinical, biological and electrophysiological described arguments could may distinguish NMM with CB from motor neuron disease and relate them to the group of chronic demyelinating neuropathies.     

Electrophysiologic findings in multifocal motor neuropathy

We performed detailed electrophysiologic studies on 16 patients with clinically defined multifocal motor neuropathy and found a wide spectrum of demyelinating features. Only five patients (31%) had conduction block in one or more nerves. However, in 15 patients (94%) at least one nerve showed other features of demyelination. We also noted a significant degree of superimposed axonal degeneration in 15 patients. Eight patients (50%) had individual nerves with pure axonal injury, despite the presence of demyelinating features in other nerves. Antiganglioside antibodies were elevated in four of five patients with conduction block and five of 11 patients without conduction block. We conclude that multifocal motor neuropathy is characterized electrophysiologically by a wide spectrum of axonal and demyelinating features. Diagnostic criteria requiring conduction block may lead to underdiagnosis of this potentially treatable neuropathy.     

Root stimulation studies in the evaluation of patients with motor neuron disease

Nerve root stimulation may be employed in patients with motor neuron disease (MND) to rule out motor neuropathy with conduction block. The diagnostic utility of these studies is unknown, in part because the range of amplitude changes across nerve root segments in patients with active neuronal degeneration has not been well studied. We reviewed root stimulation studies in 32 patients (59 nerves) with MND and found segmental amplitude reduction from 0 to 45%, a range similar to values reported for normal subjects; there was no suggestion of conduction block based on our usual criteria.     

Granulomatous orchitis. A case report and review of the literature

We developed a method for determination of motor conduction along the mandibular and sensory conduction along the lingual and inferior alveolar nerves in 10 controls and 6 patients with lingual neuropathy following lower wisdom tooth extraction. Patients with lingual neuropathy had reduced/absent or delayed compound sensory action potentials and normal conduction along the fibers of the inferior alveolar nerve and mandibular nerve. The method provides a useful electrophysiological means of evaluating lingual nerve lesions.     

Stimulation of IL-2 production and CD2R expression by splenopentin analogs

A multiplicity of peripheral nerve syndromes may develop in patients with diabetes mellitus, the commonest of which is a chronic symmetric sensory polyneuropathy, often associated with autonomic neuropathy. Once established, it is largely irreversible. Acute painful diabetic sensory neuropathy is a separate entity with a favorable prognosis. It now seems likely that chronic inflammatory demyelinating polyneuropathy occurs with greater frequency in diabetic subjects than in the general population and is one explanation for the occurrence of a predominantly motor polyneuropathy. Focal and multifocal peripheral nerve lesions are seen mainly in older diabetic patients and comprise cranial, thoracoabdominal and limb nerve lesions, the last including proximal lower limb diabetic motor neuropathy (diabetic amyotrophy). With this wide array of disorders and the frequency of diabetes, it is important to distinguish those that are directly or indirectly related to diabetes from those that have a coincidental relationship.     

Acute polyneuropathy after high dose cytosine arabinoside in patients with leukemia

BACKGROUND: Peripheral nerve toxicity has been reported but is not a commonly recognized complication of high dose cytosine arabinoside (HDAC) therapy. This study was undertaken to estimate the prevalence and describe the clinical spectrum of acute polyneuropathy associated with HDAC therapy for leukemia. METHODS: Records of 153 acute leukemia patients who received 194 courses of HDAC at the City of Hope were reviewed for evidence of severe peripheral neuropathy with onset 2-3 weeks after HDAC therapy. RESULTS: Two patients were identified who developed motor disability 2-3 weeks after HDAC therapy, and the disability progressed in a monophasic course to quadriparesis. There was neurophysiologic evidence of peripheral nerve demyelination with slowed nerve conduction velocities and conduction block. One patient who was autopsied had demyelination identified in luxol-fast blue sections of peripheral nerve (with Bielschowsky-stained sections showing intact peripheral nerve axons). There were foamy macrophages in the peripheral nerve but no chronic inflammatory cells. For comparison, data from these two patients were combined with those from four published case reports of polyneuropathy associated with HDAC therapy. Quadriparesis occurred in five of six cases with the need for ventilatory support in four. Cerebrospinal fluid protein was elevated in five of six cases. Etiologic evidence incriminating HDAC included simultaneous cerebellar signs in two of six cases and a narrow interval of clinical onset after HDAC therapy. CONCLUSIONS: Demyelinating polyneuropathy occurs in approximately 1% of HDAC courses and produces severe motor disability. HDAC immunosuppression could trigger an immune-mediated neuropathy; alternatively, a direct neurotoxic effect of HDAC on Schwann cells is also an etiologic possibility.     

Neurovascular dysfunction in diabetic rats. Potential contribution of autoxidation and free radicals examined using transition metal chelating agents

Oxygen free radical activity is elevated in diabetes mellitus and has been implicated in the etiology of vascular complications. Recent studies have shown that impaired perfusion of nerve endoneurium is a major cause of nerve fiber dysfunction in experimental diabetes. Free radical scavenger treatment prevents the development of nerve conduction abnormalities in diabetic rats. In vitro experiments suggest that autoxidation reactions of glucose, catalyzed by free transition metal ions, are a potential source of free radicals in diabetes. We investigated whether chronic treatment with deferoxamine and trientine, transition metal chelating agents which can prevent autoxidation, could correct nerve conduction and blood flow changes in streptozotocin-diabetic rats. A 20% reduction in sciatic nerve motor conduction velocity after 2 mo diabetes was 90% ameliorated by 2 wk of treatment with deferoxamine or trientine. Sciatic endoneurial nutritive blood flow was 45% reduced by diabetes, but was completely corrected by treatment. In contrast, transition metal chelation had no effect on blood flow or conduction velocity in nondiabetic rats. Thus, the data support the hypothesis that increased free radical activity by glucose autoxidation as a result of impaired transition metal handling is a major cause of early neurovascular deficits in diabetes.     

Reversal of defective nerve conduction with vitamin E supplementation in type 2 diabetes: a preliminary study

OBJECTIVE: The present study has examined the effect of vitamin E, the principal modulator of free radical activity, on electrophysiological parameters in patients with diabetic peripheral sensorimotor polyneuropathy, matched for duration of disease and metabolic control. RESEARCH DESIGN AND METHODS: A total of 21 subjects with type 2 diabetes were enrolled in this double-blind randomized placebo-controlled study (vitamin E, 11 patients; placebo, 10 patients). Patients were randomly assigned to receive either 900 mg vitamin E or placebo for 6 months. The average dietary vitamin E consumption of the subjects was similar during the study. The main outcome measure was the electrophysiological tests assessing nerve conduction. Fasting plasma glucose, HbA1, postprandial plasma glucose, and electrophysiological parameters in the basal state and after 6 months of treatment were studied. RESULTS: Glycemic indexes did not show any significant changes during the study, whereas nerve conduction improved significantly in 2 of the 12 studied electrophysiological parameters after 6 months in patients on vitamin E supplementation. The changes in the electrophysiological parameters were obvious in the median motor nerve fibers and tibial motor nerve fibers. Nerve conduction velocity in the median motor nerve fibers (P = 0.0019) and tibial motor nerve distal latency (P = 0.0284) improved significantly after 6 months of vitamin E supplementation. CONCLUSIONS: This study shows that defective nerve conduction in diabetic subjects with mild-to-moderate peripheral neuropathy may be improved by pharmacological doses of vitamin E supplementation. Further studies with a larger number of patients for longer periods of time are needed.     

Hydroxylamine blocks adenosine A1 receptor-mediated inhibition of synaptic transmission in rat hippocampus

BACKGROUND AND PURPOSE: Stroke-induced hemiparesis involving the arm and hand results in regular, repeated overuse of the opposite hand and wrist. Because repetitive hand and wrist movement is a common cause of carpal tunnel syndrome (CTS), we examined the nonparetic upper limb in stroke patients for evidence of CTS. METHODS: We measured bilaterally sensory nerve conduction velocity (SNCV), motor nerve conduction velocity (MNCV), sensory nerve action potentials (SNAP) at the wrist, palm-to-wrist distal sensory latency (DSL), palm-to-wrist SNAP, compound motor action potentials (CMAP), and distal motor latency (DML) in stroke patients and control subjects. Controls were right-handed, >/=65 years old, lucid, independent in their activities of daily living, and had no disease known to cause CTS. Stroke patients were divided into a functioning hand group (n=61) and a disused hand group (n=71). All patients had hemiplegia. RESULTS: Tinel's sign was observed on the nonparetic side in 57.7% of patients with a disused hand and in 31.1% of those with a functioning hand. All electrophysiological indices were significantly more abnormal on the nonparetic side than on the hemiparetic side or in controls. Patients with a disused hand showed greater abnormality on the nonparetic side in SNCV, SNAP, palm-to-wrist DSL, DML, and CMAP than patients with a functioning hand. CONCLUSIONS: Overuse of the nonparetic hand and wrist of the nonparetic side may result in CTS in stroke patients, especially when the paretic hand is not functional. Wrist splinting or other prophylactic treatments beginning soon after stroke might help to prevent CTS.     

Sensory and mixed nerve conduction studies in the evaluation of ulnar neuropathy at the elbow

The relative sensitivities of sensory, mixed nerve, and motor conduction studies in assessing ulnar neuropathy at the elbow have not yet been established. Using surface electrodes, we performed conduction studies across the elbow segment in 43 patients with symptoms referable to the ulnar nerve and 40 control subjects. Segmental slowing of motor conduction localized the lesion to the elbow in 14 of 21 patients (67%) with clear evidence of ulnar neuropathy on physical examination but only in 2 of 22 (9%) with subtle or no physical examination abnormalities. The diagnostic yield was increased by the finding of segmental slowing of sensory or mixed nerve conduction across the elbow to 86% and 68%, respectively, for each of the groups. We conclude that surface-recorded sensory and mixed nerve conduction studies appear to be more sensitive than motor studies in the electrodiagnosis of ulnar neuropathy at the elbow and are especially valuable in patients with subtle clinical involvement.     

Assessment of flail mitral leaflets by dynamic three-dimensional echocardiographic imaging

Patients with diabetic amyotrophy may have an inflammatory vasculopathy and may obtain reversal of neurological deficits with immunosuppression. We present a patient with NIDDM, subacute onset of painful asymmetric polyradiculopathy, and unilateral enhancement of lumbar nerve roots on MRI. Clinical improvement and resolution of nerve root enhancement occurred with immunosuppression. We suggest, therefore, that nerve biopsy and gadolinum-enhanced lumbosacral MRI be performed in all patients presenting with diabetic amyotrophy. If nerve root enhancement is present or if nerve biopsy shows perivascular infiltrates, we recommend a trial of immunosuppression.     

Insulin-like growth factor-I prevents development of a vincristine neuropathy in mice

Vincristine is a commonly used antitumor agent whose major dose-limiting side-effect is a mixed sensorimotor neuropathy. To assess whether insulin-like growth factor-I (IGF-I), a neurotrophic agent that supports the survival of motoneurons and enhances regeneration of motor and sensory neurons, could prevent the peripheral neuropathy produced by vincristine, mice were treated with both vincristine (1.7 mg/kg, i.p., 2 x /week) and/or IGF-I (0.3 or 1 mg/kg, s.c. daily) for 10 weeks. In mice treated with vincristine alone, there was evidence of a mixed sensorimotor neuropathy as indicated by changes in behavior, nerve conduction and histology. Caudal nerve conduction velocity was significantly slower in mice treated with vincristine alone as compared with vehicle-treated mice. Vincristine treatment alone also significantly increased hot-plate latencies and reduced gait support and stride length, but not toe spread distances. The effects of vincristine were accompanied by degeneration of sciatic nerve fibers and demyelination, indicating a peripheral neuropathy. IGF-I (1 mg/kg, s.c.) administered to vincristine-treated mice prevented the neurotoxic effects of vincristine as measured by nerve conduction, gait, response to noxious stimuli and nerve histology. At a lower dose of 0.3 mg/kg administered s.c., IGF-I partially ameliorated the neuropathy induced by vincristine as this dose only prevented the change in nerve conduction and hot-plate latencies. IGF-I administered alone had no effect on any of these parameters. These results suggest that IGF-I prevents both motor and sensory components of vincristine neuropathy and may be useful clinically in preventing the neuropathy induced by vincristine treatment.     

Multifocal motor neuropathy

We present a review of the literature on multifocal motor neuropathy (MMN), a rare neurological disorder which has features in common with both chronic inflammatory demyelinating neuropathy and lower motor neuron disease. Clinically, MMN is characterised by slowly progressive asymmetrical limb weakness, usually most prominent in the forearms. Weakness may be associated with muscle wasting, fasciculations and decreased tendon reflexes. Serum anti-GM1 ganglioside antibody titres may be increased. The diagnostic hallmark of MMN is the electrophysiological demonstration of persistent localised motor conduction blocks, with otherwise normal or near-normal motor and sensory conduction velocities. The pathogenesis of MMN has not been elucidated completely. There is, however, substantial evidence for an autoimmune mechanism. Based on the possible involvement of the immune system in the pathogenesis of MMN the therapeutic efficacy of several immunomodulatory drugs has been tested. Treatment of MMN patients with human immunoglobulin or cyclophosphamide is usually followed by a marked improvement of strength. The finding that MMN is a potentially treatable disorder underscores the importance of distinguishing MMN from lower motor neuron disease, for which no effective therapy is currently available.     

Peripheral nervous system involvement in human and experimental chronic American trypanosomiasis

An electrophysiological and histological study of the muscle and the peripheral nervous system (PNS) was carried out in chronic human American trypanosomiasis (Chagas' disease) and in an experimental Chagas' disease (Chd) mouse model. Altogether 995 patients with chronic Chd and 261 mice, experimentally infected with RA and CA-I parasite strains, were investigated. Results were compared with matched controls. Techniques employed in humans were: clinical assessment, conventional electromyography (EMG), estimated number of motor units, motor and sensory nerve conduction velocities, repetitive nerve stimulation and muscle and sural nerve biopsies. In mice conventional EMG, sciatic nerve conduction time, sciatic nerve action potential amplitude, in vitro miniature end-plate potentials (MEPPs) and end-plate potentials (EPPs) recordings, muscle, nerve and spinal cord histology and identification of cell phenotypes within the inflammatory infiltrates were the employed procedures. Out of 511 patients submitted to clinical examination, 52 disclosed signs and symptoms of mixed peripheral neuropathy. By employing electrophysiological techniques, it could be shown that about 30% of the investigated patients had one or more of the following features: diminished interference pattern, most of the remainder motor unit potentials being (MUPs) polyphasic; reduced number of functional motor units in the thenar, hypothenar, soleus and/or edb muscles; slow sensory and motor nerve conduction velocities; low sensory action potential amplitude and impairement of neuromuscular transmission. In mice, MUPs duration and amplitude were increased at later stages of the infection, nerve conduction was slow, nerve action potentials were of low amplitude, mepps were of low amplitude and double epps were frequently found. Muscle histology in humans with chronic Chd showed type I and type II grouping, atrophic angular fibers and targetoid muscle fibers. In mice perivascular mononuclear cells infiltrates, small round fibers, muscle fibers necrosis, atrophic angular fibers, type II muscle fibers grouping and grouped muscle fibers atrophy were found. Sural nerve samples showed segmental and paranodal demyelination and axonal loss. The same features were observed in mice nerves, also in this model mononuclear cells infiltrates at the nerve, dorsal root ganglia and meninges surrounding the spinal cord were observed. Muscle and nervous tissues infiltrates were mainly composed of T lymphocytes with predominance of CD8 or CD4 subsets according to the parasites strain employed for infecting the animals. These findings suggest that the skeletal muscle and the PNS may be involved in chronic American trypanosomiasis.     

Treatment of acquired von Willebrand syndrome in patients with monoclonal gammopathy of uncertain significance: comparison of three different therapeutic approaches

Patients with monoclonal gammopathies of uncertain significance (MGUS) may develop an acquired bleeding disorder similar to congenital von Willebrand disease, called acquired von Willebrand syndrome (AvWS). In these patients, measures to improve hemostasis are required to prevent or treat bleeding episodes. We diagnosed 10 patients with MGUS and AvWS: 8 had IgGkappa (3) or lambda (5) MGUS and 2 IgM-kappa MGUS. Three therapeutic approaches were compared in them: (1) desmopressin (DDAVP), (2) factor VIII/von Willebrand factor (FVIII/vWF) concentrate, and (3) high-dose (1 g/kg/d for 2 days) intravenous Ig (IVIg). In patients with IgG-MGUS, DDAVP and FVIII/vWF concentrate increased factor VIII and von Willebrand factor in plasma, but only transiently. IVIg determined a more sustained improvement of the laboratory abnormalities and prevented bleeding during surgery (short-term therapy). In addition to the standard 2-day infusion protocol, a long-term IVIg therapy was performed in 2 patients with IgG-MGUS: repeated (every 21 days) single infusions of IVIg did improve laboratory abnormalities and stopped chronic gastrointestinal bleeding. On the other hand, IVIg failed to correct laboratories abnormalities in patients with IgM-MGUS. These comparative data obtained in a relative large and homogeneous group of patients with AvWS and MGUS confirm that DDAVP and FVIII/vWF concentrates improve the bleeding time (BT) and FVIII/vWF measurements only transiently, whereas IVIg provides a sustained treatment of AvWS associated with IgG-MGUS, but not with IgM-MGUS.     

Can motor recovery in stroke patients be predicted by early transcranial magnetic stimulation?

BACKGROUND AND PURPOSE: We used transcranial magnetic stimulation of the motor cortex to evaluate the functional state of corticospinal pathways innervating the first dorsal interosseous muscle of the hand in 26 patients suffering from a first-ever ischemic stroke in the middle cerebral artery territory. METHODS: All patients had complete hand palsy and were tested within the first 24 hours from stroke onset. Patients were also tested clinically with the MRC, Rankin, and National Institutes of Health (NIH) stroke scales at day 1 and with MRC and NIH scales and the Barthel Index at day 14. Electrophysiological testing was repeated at day 14. Patients were divided into three subgroups according to the amplitude of the maximal response (motor evoked potential [MEP]) evoked at day 1. RESULTS: After 2 weeks, all 6 patients with initial MEPs > 5% maximum motor response (Mmax) showed some first dorsal interosseous muscle motor function recovery, whereas 19 of 20 patients with initially absent or small (< 5% Mmax) MEPs were left with complete hand palsy. There were strong positive correlations between MEP amplitude at day 1 and MRC and Barthel Index scores at day 14. However, measurement of central motor conduction time proved to be of little prognostic value. CONCLUSIONS: We conclude that early-performed transcranial magnetic stimulation is a valuable prognostic tool for motor recovery from stroke and that relatively preserved MEP amplitude shortly after stroke is a better prognostic factor than normal central motor conduction time.