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Objectives: Statins have anti–inflammatory effects on several neurological diseases. However, their effects on post-stroke epilepsy and mortality have not been well studied.Method: This is a retros...

This post hoc analysis assessed the long-term safety, tolerability, and efficacy of perampanel in Asian patients with refractory focal seizures; an additional analysis assessed the effect of perampanel on focal impaired awareness seizures (FIAS) with focal to bilateral tonic-clonic (FBTC) seizures. In this subanalysis, data from Asian patients ≥12 years of age who had focal seizures with FBTC seizures despite taking one to 3 concomitant antiepileptic drugs at baseline, and who had entered either the long-term extension phase of 3 phase-3 perampanel trials (study 307) or the 10-week extension phase of study 335, were analyzed for the effect of perampanel on duration of exposure, safety, and seizure outcomes. Of 874 Asian patients included in the analysis, 205 had previously received placebo during the double-blind phase-3 trials and 669 had previously received perampanel 2-12 mg/day; 313 had FIAS with FBTC seizures at core study baseline. The median duration of exposure to perampanel was 385.0 days, and the retention rate at one year was 62.6%. Overall, during the first 52 weeks of perampanel treatment, 777 patients (88.9%) had treatment-emergent adverse events (TEAEs), most of which were mild to moderate in severity. The most frequent TEAEs were dizziness (47.1%), somnolence (22.3%), and nasopharyngitis (17.4%). During the first 52 weeks of perampanel treatment, median percent change in seizure frequency per 28 days from pre-perampanel baseline for all focal seizures was -28.1%, and -51.7% for FIAS with FBTC seizures. The 50% responder rate relative to pre-perampanel baseline for all focal seizures was 33.8%, and 51.1% for FIAS with FBTC seizures. Long-term treatment with perampanel in Asian patients had safety, tolerability, and efficacy similar to that of the global population in the phase-3 trials and extension study 307. The safety profile and response rate suggest benefit for an Asian population of patients with refractory epilepsy.

Rationale Lacosamide (LCM) was initially approved in Taiwan in March 2014 for use as adjunctive therapy for focal impaired awareness seizures and secondarily generalized seizures (SGS) in patients with epilepsy ≥ 16 years of age. The efficacy and tolerability of adjunctive LCM for the treatment of patients with focal seizures have been demonstrated in randomized, placebo-controlled trials. However, the trials do not reflect a flexible dose setting. This study (EP0063) was conducted to assess the safety and tolerability of LCM in real-world clinical practice in Taiwan. Effectiveness of LCM was also assessed as an exploratory objective. Methods EP0063 was a multicenter, prospective, noninterventional study with an expected observation period of 12 months ± 60 days. Eligible patients were ≥ 16 years of age, had focal impaired awareness seizures and/or SGS (in line with approved indication in Taiwan at the time of the study), were taking at least one concomitant antiseizure medication (ASM), and had at least one seizure in the 3 months before baseline. Patients were prescribed LCM by their treating physician in the course of routine clinical practice. The primary safety variable was treatment-emergent adverse events (TEAEs) spontaneously reported to, or observed by, the treating physician. Based on safety data from previous studies of LCM and known side effects of other ASMs, certain TEAEs (including but not limited to cardiac and electrocardiogram, suicidality, and rash related terms) were analyzed separately. Effectiveness variables included Clinical Global Impression of Change (CGIC) and change in 28-day seizure frequency from baseline to 12 months (or final visit), and freedom from focal seizures. Results A total of 171 patients were treated with LCM, of whom 139 (81.3%) completed the study. The Kaplan–Meier estimated 12-month retention was 82.9%. Patients had a mean (standard deviation [SD], range) age of 38.5 (14.0, 16–77) years, and 96 (56.1%) were male. Patients were taking a mean (SD, range) of 2.8 (1.1, 1–6) ASMs at baseline. Mean (SD, range) duration of LCM treatment was 288.7 (111.9, 2–414) days, and the mean (SD, range) daily dosage of LCM was 205.0 (82.7, 50.0–505.2) mg/day. Overall, 95 (55.6%) patients reported at least one TEAE, most commonly dizziness (33 [19.3%] patients). Drug-related TEAEs were reported in 74 (43.3%) patients, and drug-related TEAEs leading to discontinuation of LCM were reported in 14 (8.2%) patients. Two (1.2%) patients died during LCM treatment, which were considered not related to LCM. Two (1.2%) patients had suicidality-related TEAEs; these TEAEs were considered either not related to LCM or the relationship was not recorded. Rash-related TEAEs were reported in five (2.9%) patients (considered LCM-related in two patients). Based on the CGIC, at 12 months (or final visit), 109 (63.7%) patients were considered to have improved, 54 (31.6%) had no change, and the remaining eight (4.7%) were minimally worse. At 12 months (or final visit), the median percentage change in focal seizure frequency was –50.0. During the first 6 months of the study, 21 (12.3%) patients were free from focal seizures; 37 (21.6%) patients were free from focal seizures in the last 6 months of the study; and 14 (8.2%) were free from focal seizures for the full 12 months of the study. Conclusions Results of this prospective, noninterventional study suggest that adjunctive LCM was generally safe and well tolerated in this patient group in real-world practice in Taiwan. Effectiveness was also favorable, with more than 60% of patients considered to be improved by their physician at 12 months (or final visit).

Transarterial chemoembolization (TACE) plays an essential role in the management of unresectable hepatocellular cell carcinoma and other hepatic neoplasms. Cerebral lipiodol embolism (CLE) is a rare complication of TACE and its prognostic factors have not been well studied. The aim of this paper was to elucidate the prognostic factors of CLE based on clinical data obtained from our patients and cases published since 2004.We present two patients with CLE, analyze the clinical data, and review all CLE cases published since 2004. A poor outcome was defined as stupor, coma, quadriplegia, or death within 45 days. Patients who had other neurological conditions within 45 days were considered as having a good outcome.The rate of poor outcome was 25.7% (9/35). Compared with the patients with good outcome, those with poor outcome were older (mean age 68.3 ± 7.3 vs. 58.3 ± 10.6 years, p = 0.03), more often female (76.9% vs. male 33.3%, p = 0.02), and more likely chemoembolized via both the right hepatic and right inferior phrenic arteries (44.4 vs. 8.7%, p = 0.02).The prognosis of CLE was related to age, gender, and the arteries selected for injection.

Occipital lobe seizures caused by nonketotic hyperglycemia (NKH) have been reported in only a few cases and are not fully characterized. We report two cases of NKH-related occipital lobe seizures with high hemoglobin A1C (HbA1C), epileptiform electroencephalograph (EEG) and MRI abnormalities. Both patients had moderate hyperglycemia (310–372mg/dl) and mildly elevated serum osmolarity (295–304mOsm/kg) but markedly elevated HbA1C (13.8–14.4%). One patient had a clinico-EEG seizure originating from the right occipital region during sleep. The other patient had an interictal epileptiform discharge consisting of unilateral occipital beta activity in sleep. None of the previously reported cases fulfilled the criteria of a nonketotic hyperglycemic hyperosmolar (NKHH) state, or showed any interictal beta paroxysms, spikes, sharp waves, or spike/sharp-slow wave complexes. We suggest that prolonged exposure to uncontrolled hyperglycemia, as indicated by HbA1C, rather than an acute NKHH state is crucial in the development of this peculiar seizure. We also suggest clinicians look for the presence of interictal focal beta paroxysms in addition to the usual epileptiform discharges while reading the EEG of these patients.

Parkinsonian variant of multiple system atrophy (MSA-P) clinically presents as autonomic dysfunction with parkinsonian features. Parkinsonian features include bradykinesia, rigidity, tremor, postural instability and poor levo-dopa response. Neuropathologically, MSA-P is characterized by selective neuronal loss and gliosis mainly affecting the putamen and caudate nucleus, substantia nigra, olivopontocerebellar pathway and intermediolateral cell column of the spinal cord. Therefore, the target of magnetic resonance imaging (MRI) is focused on signal changes or volume reduction on putamen, including putaminal slit, gliosis by diffusion studies and reduction of putaminal volume. There have been no reports describing clinical manifestations of MSA-P with imaging abnormalities over globus pallidus. Here, we describe three patients with typical presentations of MSA-P with autonomic dysfunction and disturbances of axial motor function with minimal appendicular symptoms, including postural instability and gait difficulties. MRI showed symmetrical hyperintensity over the center of globus pallidus surrounded by a mild low-signal rims at T2-weighted image that is similar to that of eye of the tiger sign except for the marked hypointense rims. Dopamine transporter scans showed symmetric reduction of uptake over bilateral basal ganglia. This is the first report concerning these unusual imaging findings in MSA-P patients and we believe there is a subgroup of MSA-P with clinical presentation of axial impairment and symmetrically abnormal signal changes of globus pallidus in MRI.

The decrease of forearm median motor conduction velocity (CV) in carpal tunnel syndrome (CTS) is a common electrodiagnostic finding in clinical practice and is possibly secondary to either conduction block at wrist or retrograde conduction slowing (RCS). This study is attempted to confirm the existence of RCS and to explore why this controversy occurs for a long time. Eighty CTS patients and controls were recruited. In addition to conventional electrodiagnosis, subjects received further electrodiagnostic protocol. First, a recording electrode was placed over the wrist and then at elbow with palm stimulation to calculate indirect forearm mixed nerve CV (forearm-mix CV) that represented real measurement of nerve fibers through the carpal tunnel. Then, direct measurement of forearm-mix CV was performed with recording at the elbow and stimulation at the wrist. CTS patients had markedly prolonged distal motor and sensory latencies and significantly prolonged wrist-palm sensory and motor conduction. There was a significant decrease in forearm median motor CV; however, there was no difference in ulnar distal motor latency and forearm motor CV. The mild decrease of forearm median motor CV was not proportional to the marked reduction of W-P MCV and there was no demonstrated conduction block at wrist, implying the reduction of forearm median motor CV is unlikely due to conduction blockage or slowing of the large myelinating fibers at the wrist and RCS really occurs over the forearm median nerve. In addition, the direct Forearm-mix CV was similar in CTS and controls; however, there was a significant decrease in indirect forearm-mix CV only in the CTS. Moreover, the difference between direct and indirect forearm-mix CV was significantly greater and poor consistency of direct and indirect forearm-mix CV in CTS, suggesting that direct and indirect forearm-mix CV represent CV from quite different nerve fibers. Therefore, we conclude that RCS really does occur in CTS and the direct forearm-mix CV reflects the CV of nerve fibers without damage in CTS. The misinterpretation and measurement of different components of forearm-mix CV results in the existence of this controversy till now.

The objective of this study was to determine the cause of median forearm motor conduction velocity (FMCV) slowing in patients with carpal tunnel syndrome, due to either focal conduction abnormality over wrist or retrograde conduction slowing, and to decide whether the slowing is related to severity of compression or not. Fifty carpal tunnel syndrome patients confirmed by conventional nerve conduction study with abnormal electromyography of the abductor pollicis brevis muscle were group 1, and 100 with normal electromyography, group 2. One hundred volunteers served as controls. In addition to conventional nerve conduction study of median and ulnar nerves, palmar stimulations for median mixed and motor nerves were also performed to calculate wrist-palm mixed nerve conduction time and motor conduction velocity (W-P MCV). For group 1, group 2, and control subjects, respectively, W-P MCV were 19.73+/-7.65 (mean+/-SD), 32.7+/-6.83, and 52.75+/-6.4 m/s, whereas median FMCV were 48.63+/-8.32, 54.42+/-2.11, and 57.86+/-4.24 m/s. There was a significant reduction in the W-P MCV (62.6%, P

Objective To compare the sensitivity of median wrist–palm motor conduction velocity (W–P MCV) with those of standard sensory conduction techniques in the electrodiagnosis of carpal tunnel syndrome (CTS). Methods This study included 280 consecutively suspected CTS patients (360 hands) referred for evaluation and 150 volunteers who served as controls. We determined and calculated (1) median W–P MCV, (2) median motor distal latencies (DL) and median sensory DL for (3) thumb (D1), (4) index (D2) and (5) ring finger (D4), (6) median wrist–palm sensory conduction velocity (W–P SCV) and sensory conduction time (W–P SCT) for index finger and sensory latency differences between (7) median–radial (M–R) for thumb and (8) median–ulnar (M–U) nerves for ring finger. The normal limits were calculated from the median of normal controls ±2.5 standard deviations. The sensitivities of each test were determined and compared. Results Among the 360 hands with suspected CTS, 32 hands (8.9%) had normal electrodiagnostic studies and 328 (91.1%) had at least one abnormal electrodiagnostic study. Among the 328 hands with abnormalities, 234 (65%) had abnormal motor DL and 294 (81.7%) had abnormal W–P MCV. The sensitivity was 80.3% for D1, 72.5% for D2, 76.7% for D4, 86.7% for M–R (specificity, 98.7%), 87.2% for M–U (specificity, 96.7%), 80.8% for sensory W–P SCT and 73.6% for W–P SCV. Conclusions W–P MCV is a valuable motor conduction technique for the diagnosis of CTS and it is confirmed again that W–P MCV is equal to or more sensitive than W–P SCV and W–P SCT. Furthermore, the findings of the present study are in agreement with the conventional wisdom that internal comparison of latency differences between median and ulnar or radial nerves is the best method for a diagnosis of patients with suspected CTS. Therefore, we recommend that CTS patients be studied according to the following steps: (1) routine sensory and motor DL, (2) if step 1 is negative, then perform and determine W–P MCV or SCT. This may increase the diagnostic yield of 10%, (3) if step 2 is negative, measure the M–U or MR. These are the final and more sensitive techniques in making a diagnosis with an additional diagnostic yield of 10%. Significance We provide the evidence of W–P MCV that could be a standard technique for electrodiagnosis of CTS. Furthermore, we make a reasonable flow chart and recommendation for electrodiagnosis of CTS for electromyographers.

Summary: Purpose: Hyperglycemia may rarely be seen with visual seizures. Observation of both visual evoked potentials (VEPs) and magnetic resonance imaging (MRI) in visual status epilepticus (SE) has not been reported. We describe acute and follow-up VEP and MRI findings of a patient with hyperglycemia-related visual SE of occipital origin. Methods: In a 59-year-old diabetic woman, complex visual hallucinations and illusions developed with ≤10 seizures per hour as an initial manifestation of nonketotic hyperglycemia. Results: Neurologic examination revealed ictal nystagmus to the right and continuous right hemianopsia. Ictal electroencephalography (EEG) and Tc-99m hexamethylpropylene amine oxime (HMPAO) single-photon emission computed tomography (SPECT) revealed an epileptogenic focus in the left occipital lobe. MRI with fluid-attenuated inversion recovery showed focal subcortical hypointensity and gyral hyperintensity. Followup MRI showed only minimal gyral hyperintensity at 6 months. The P100 amplitude of VEP was significantly higher at the right occipital area during SE, but slightly higher on the left after the patient had been seizure free for 6 months. Conclusions: Occipital seizures and hemianopsia can be caused by hyperglycemia and may be accompanied by special MRI and VEP findings. Ke yW ords: Nonketotic hyperglycemia—Hemianopsia—Visual evoked potentials— Magnetic resonance imaging.

The cause of decreased median forearm motor conduction velocity (FMCV) in carpal tunnel syndrome (CTS) is best ascribed to retrograde axonal atrophy (RAA); however, the relationships between the occurrence of RAA and electrophysiological or clinical severity remains controversial. We attempt to determine whether RAA really occurs in CTS patients with normal median FMCV and to investigate any relationships between RAA and severity of compression at the wrist.Consecutive CTS patients were enrolled and age-matched volunteers served as controls. We performed conventional nerve conduction studies (NCS) and measured median and ulnar distal motor latencies (DML), FMCV, compound muscle action potential (CMAP) amplitudes, distal sensory latencies (DSL), and sensory nerve action potential (SNAP) amplitudes. Furthermore, palmar median stimulation was done to calculate the wrist-palm motor conduction velocity (W-P MCV). Patients included for analysis should have normal FMCV and needle examination. We compared each electrodiagnostic parameters between the patient group and controls.The mean+/-SD of the W-P MCV for patients and controls were 33.26+/-6.74 and 52.14+/-5.85 m/s and those of median FMCV were 55.26+/-3.56 and 57.82+/-3.9 m/s, respectively. There was a significant reduction in the W-P MCV (36.2%, P0.00001), significant decrease in the median FMCV (4.43%, P0.00001) and SNAP amplitudes, and an increase of the DML and DSL in the patient group (P0.00001) compared to the controls; however, there were no differences in median and ulnar CMAP amplitudes, ulnar FMCV and DML between the controls and patients.RAA and relatively slowed median FMCV do occur in CTS patients with normal median FMCV, regardless of severity of clinical manifestations and electrophysiological abnormalities.This article provides new information for research of the electrophysiological changes of the proximal nerve part at distal injury.

Objectives : The purpose of this study was to determine whether forearm (wrist–elbow) mixed nerve conduction velocity (W–Emix) represents the actual nerve conduction velocity (CV) of nerve fibers passing through the carpal tunnel. Background : W–Emix is presumed to reflect the actual forearm CV through the carpal tunnel. However, it has been argued that W–Emix chiefly originates from the nerve fibers passing outside the carpal tunnel. Therefore, the direct measurement of W–Emix cannot be used to assess retrograde axonal atrophy in carpal tunnel syndrome (CTS). Subjects and methods : Thirty patients with clinical signs and symptoms of CTS were recruited and the diagnosis was confirmed with standard electrodiagnosis. Fifty age-matched volunteers served as control. Recording electrodes were placed over the elbow and index finger for mixed nerve and sensory nerve conduction studies, respectively. Stimulation was applied at the palm and wrist for the measurement of mixed nerve wrist–palm CV (W–Pmix), wrist–elbow CV (W–Emix), and elbow–palm CV (E–Pmix). Stimulation was applied at the elbow, wrist, and palm for the measurement of wrist–elbow sensory CV (W–Esen), wrist–palm CV (W–Psen), and elbow–palm CV (E–Psen). Comparisons were made between W–Pmix and W–Psen, W–Emix and W–Esen, and E–Pmix and E–Psen. Results : Correlations between W–Emix and W–Esen, E–Pmix and E–Psen, and W–Pmix and W–Psen were good in the control. In the patient group, there was a strong positive correlation between W–Pmix and W–Psen, and between E–Pmix and E–Psen. However, W–Esen correlated weakly with W–Emix, suggesting that W–Emix chiefly represents the CV of fibers passing outside the carpal tunnel. Therefore, the direct measurement of W–Emix cannot be used to assess retrograde axonal atrophy. Furthermore, the reduction in W–Psen was more marked than the reduction in W–Esen, implying that a conduction block at the wrist is the least likely cause of proximal slowing in CTS. Conclusions : W–Emix does not reflect the actual CV of the nerve fibers passing through the carpal tunnel. In addition, retrograde axonal atrophy appears to be the primary cause of decreased forearm CV in CTS.

Neuronal damage in relation to the duration of seizure was studied in limbic status epilepticus (SE) induced by electric stimulation of naive rats. Adult Sprague-Dawley rats were stimulated at the right amygdala to induce SE. To stop the seizures, diazepam was given to different groups of rats at 0.5 h (n = 4), 1 h (n = 6), 2 h (n = 6), and 3-4 h (n = 8) of SE. Eighteen hours after the end of SE, the rats were perfusion fixed. Naive (n = 6) and sham-operated (n = 4) rats served as controls. Horizontal paraffin sections were stained with acid fuchsin and cresyl violet. Neuronal damage was absent after 30 min of SE. Status epilepticus of 1 h or longer duration regularly caused neuronal damage to the cerebral cortex, thalamus, hippocampus, amygdala, and pars reticulata of the substantia nigra. Damage in the cerebral cortex predominated in the entorhinal, temporal, and pyriform regions. In the hippocampus, the dentate hilus was most severely affected, followed by CA3 and CA1. Damage to the dentate granule layer was mild. Further studies of the pathophysiology of excitotoxicity may help to protect patients from sequels of status epilepticus such as neuronal damage and epilepsy.

Transcarpal conduction techniques are commonly used to be supplementary techniques to distal sensory and motor latencies (DSL and DML) in the electrodiagnosis of carpal tunnel syndrome (CTS). However, which transcarpal conduction techniques, or combination of techniques, are the most sensitive for the electrodiagnosis of CTS is unknown. To determine which transcarpal conduction technique is the most sensitive for the electrodiagnosis of CTS, we prospectively conduct this study. Study subjects were 100 patients with CTS and 50 controls. In addition to DSL and DML determinations, all subjects were evaluated using four transcarpal conduction techniques. These were (1) median wrist-palm sensory conduction time (W-Psen CT); (2) median wrist-palm mixed nerve conduction time (W-Pmix CT); (3) the difference of conduction time across wrist between median and ulnar nerves (W-Pmix M-U CT); and (4) median wrist-palm motor conduction velocity (W-Pmot CV). The sensitivities and specificities of these tests were compared. Ninety patients had one or more electrophysiologic abnormalities. The DSL and DML diagnostic sensitivities were 74% and 72%, respectively. Better sensitivities were obtained with W-Psen CT (82%), W-Pmot CV (81%), W-Pmix CT (78%), and W-Pmix M-U CT (79%). Compared between four transcarpal conduction techniques, there was no significant difference in sensitivity. Of 26 patients with CTS with normal DSL, additional electrophysiologic abnormalities were revealed with W-Psen CT (30.7%), W-Pmot CV (53.8%), W-Pmix CT (30.7%), or W-Pmix M-U CT (38.5%). When W-Pmot CV was compared with W-Psen CT and W-Pmot CV versus W-Pmix CT, calculated probabilities (P = 0.07) showed a clear trend toward statistical significance. Furthermore, of 20 patients with normal DSL and DML, five patients had abnormality for W-Psen CT, eight for W-Pmot CV, four for W-Pmix CT, and six for W-Pmix M-U CT. On the basis of the results, we concluded that the most simple and reliable transcarpal conduction for electrodiagnosis of CTS was W-Psen CT. The most sensitive technique was W-Pmot CV in subjects with normal DSL or with normal DSL and DML. Evaluation of transcarpal motor conduction affords a useful supplementary technique to W-Psen CT.

Objective A decrease of forearm median motor conduction velocity (CV) is a common electrophysiological finding in carpal tunnel syndrome (CTS), ascribed to two possible mechanisms: either conduction block or slowing of the fastest myelinating fibers in the carpal tunnel, or retrograde axonal atrophy (RAA) with retrograde conduction slowing (RCS). We hope to utilize both direct and derived forearm median mixed nerve conduction studies to clarify the mechanism of the decrease of forearm median motor CV in CTS. Methods Seventy-five CTS patients and 75 age-matched control subjects received conventional motor and sensory nerve conduction studies of median and ulnar nerves and forearm median mixed nerve conduction techniques. First, direct measurement of forearm median mixed conduction velocity (Forearm mixed CV) and nerve action potential amplitude (Forearm mixed amplitude) was determined with recording at elbow and stimulation at wrist. Then, stimulating electrode was placed over palm and recording at elbow and then at wrist to calculate the derived Forearm mixed CV. Electrophysiological parameters, including direct Forearm mixed CV and amplitude and derived Forearm mixed CV, were compared between CTS patients and controls. Results CTS patients had significantly prolonged wrist–palm sensory and motor conduction, significantly decreased forearm median motor CV, and normal ulnar nerve conduction. The direct Forearm mixed amplitude was significantly decreased in CTS patients. The direct Forearm mixed CV was similar in CTS patients and controls, but there was a significant decrease in derived Forearm mixed CV in CTS group. The difference between direct and derived Forearm mixed CV was significantly greater in the CTS, suggesting that direct and derived Forearm mixed CV represent CV from different nerve fibers, one passing outside carpal tunnel without undergoing RAA or the other through the carpal tunnel with occurrence of RAA. Conclusion A decrease of direct Forearm mixed amplitude really occurs in CTS, implying that RAA and RCS will develop over proximal median nerve at distal nerve injury and the decreased forearm median motor CV is best ascribed to RAA and RCS. Furthermore, in CTS, the direct Forearm mixed CV measures the CV from undamaged nerve fibers without passing through carpal tunnel, resulting in the misinterpretation of the cause of proximal conduction slowing secondary to conduction block or slowing over the wrist. Significance We provide a direct evidence of the occurrence of RAA and RCS that would explain the cause of proximal median nerve conduction slowing. However, the clinical significance of RAA and RCS is uncertain.

The objective of this study was to determine whether forearm mixed nerve conduction velocity (Fmix) reflects the real conduction velocity of forearm motor nerve (Fmot) and forearm sensory nerve (Fsen) fibers passing through the carpal tunnel. Forearm mixed nerve conduction velocity is presumed to be indicative of the conduction velocity of the median nerve over the forearm. Therefore, Fmix is used widely to assess the causes of slowing forearm conduction velocity in carpal tunnel syndrome. However, some authors claim that Fmix comes chiefly from the undamaged fibers in carpal tunnel syndrome, and thus cannot replace Fmot or Fsen in the evaluation of retrograde axonal atrophy. Patients with clinical symptoms and signs of carpal tunnel syndrome confirmed with standard electrodiagnosis were included. Age-matched volunteers served as control subjects. Conduction velocities across the wrist and over the forearm were measured, including those of the wrist sensory (Wsen), wrist motor (Wmol), and wrist mixed nerves (Wmix); and forearm mixed (Fmix), forearm motor (Fmot), and forearm sensory nerves (Fsen). The authors compared and correlated Wsen, Wmot, and Wmix; and Fmix, Fmot, and Fsen respectively. The mean values of Wsen, Wmot, Wmix, Fmix, Fmot, and Fsen of the control subjects less those of corresponding conduction velocity of carpal tunnel syndrome patients were designated Wsen N, Wmot N, Wmix N, Fmix N, Fmot N, and Fsen N respectively and were compared and correlated again. Wrist motor nerve conduction velocity, Wsen, and Wmix were significantly lower in carpal tunnel syndrome patients, and Fmot and Fsen but not Fmix were reduced significantly when compared with control subjects. Mean wrist sensory nerve conduction velocity. Wmot N, and Wmix N; and Fsen N and Fmot N showed good correlation except for Fmix N, suggesting that Fmix reflects the conduction velocity of undamaged fibers in carpal tunnel syndrome. Forearm mixed nerve conduction velocity cannot replace Fmot or Fsen in the assessment of retrograde axonal atrophy in carpal tunnel syndrome. In the disease state, Fmix possibly represents the conduction velocity of the palmar cutaneous branch.

The relation between clinical outcome and single photon emission tomography (SPECT) results in cerebellitis has not been studied. A 63-year-old man developed cerebellar dysfunction with left emphasis one week after onset of cough. The only abnormality on analysis of cerebrospinal fluid was elevated protein (68 mg/dl). Magnetic resonance imaging was normal on the ninth day of ataxia. SPECT showed unilateral cerebellar hypoperfusion on the 13th day, but was normal on the 20th day. His gait improved a little by discharge on the 28th day and his tandem gait was only slightly unsteady six months later. This is the first evidence that normalization of cerebellar hypoperfusion in adult patients with cerebellitis is related to good outcome. Normalization of cerebellar hypoperfusion can occur in three weeks even when ataxia remains severe.

Objectives : To elucidate the etiopathogenesis of decreased forearm median motor conduction velocity (FMMCV) in carpal tunnel syndrome (CTS), we used segmental stimulation at the palm, wrist and antecubital fossa to determine conduction block at wrist and calculate and compare the segmental median motor conduction velocity (MMCV) to determine the pathogenesis. Background : The cause of the decreased FMMCV in CTS remains unclear. Animal models have supported retrograde axonal atrophy as the cause. Some authors believe standard FMMCV, calculated by subtracting the distal latency, may not represent an exact assessment of FMMCV but rather the velocity of small fibers that persist throughout the carpal tunnel. Subjects and methods : Patients with clinical symptoms and signs of CTS which had been confirmed with standard electrodiagnosis, were included. The patients were divided into two groups: one with reduced FMMCV n =20) and the other with normal FMMCV>50m/s (Group II, n =40). Age-matched volunteers served as controls ( n =60). We used palm, wrist and antecubital stimulation, and recorded compound muscle action potential (CMAP) amplitudes at the abductor pollicis brevis (APB) muscle. Based on a ratio of the CMAP amplitudes obtained from wrist and palm stimulation (W/P ratio) and the latency differences, we calculated the W/P ratio and the across wrist MMCV (AWMMCV) and FMMCV and compared and correlated them between two patient groups. Results : There was no difference in median motor and sensory distal latency between Groups I and II. CMAP and sensory nerve action potential amplitudes were reduced in Group I compared with Group II, but the difference was only marginally significant. Four patients had a significant reduction of the W/P ratio in Group I, compared with 7 patients in Group II, which did not reach a significance. Sixteen patients (80%) in Group I demonstrated no conduction block. Furthermore, Group I showed significantly decreased FMMCV when compared with Group II; however, AWMMCV was not significantly reduced in Group I, suggesting that decreased FMMCV does not result from a decrease in AWMMCV. Conclusions : There was no significant motor conduction block and no correlation of the FMMCV and AWMMCV in CTS patients with a decrease of FMMCV, suggesting retrograde axonal atrophy, and not selective conduction block of the large fibers at the wrist, is the direct cause of decreased FMMCV in CTS.