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We report a case of brain infarction in the anterior choroidal artery territory accompanied homonymous scotomas. A 59-year-old man with diabetes mellitus felt weakness in his left upper and lower extremities. He was admitted to our hospital with mild hemiparesis on his left side. He noticed a small black spot in the left inferior portion of his visual field; however, this disappeared within one minute. He had no visual defects as assessed by a confrontation test, but a Goldmann visual field test revealed that there were homonymous scotomas in the left inferior portion of the visual field. Brain MRI showed hyperintense signals on diffusion-weighted images in the territory of the right anterior choroidal artery. He was diagnosed as having a brain infarction. The anterior choroidal artery penetrates the lateral geniculate nucleus from the front, and branches of the artery usually supply the medial and lateral parts of the lateral geniculate nucleus. Occlusion of these branches causes the loss of the upper and lower homonymous sectors in the visual field. The present case exhibited homonymous scotomas. We assumed that our patient's homonymous scotomas were a variant form of wedge-shaped visual field deficits often seen in anterior choroidal artery syndrome. On the basis the experience gained in this case, we consider that patients with brain infarction in the anterior choroidal artery territory should undergo ophthalmological examination, even when no visual defects are detected by a confrontation test.

The patient was a 31-year-old woman in whom facial paralysis occurred 1 week after the onset of pyelonephritis. Peripheral facial paralysis, sensorineural deafness, dysarthria, weakness of the four limbs, loss of tendon reflex, and peripheral sensory disturbance of the four limbs were noted during the initial examination. These symptoms were dominant in left side. The number of cells and protein level were increased in the cerebrospinal fluid, and reduced motor nerve action potential was detected with peripheral nerve conduction test. Based on these findings, axonal Guillain-Barré syndrome (GBS) was diagnosed. Left side-dominant bilateral hypoacusia was noted with audiogram, and left side-dominant bilateral prolongation of I wave latency was noted with auditory brainstem response (ABR). The ABR findings indicated that the auditory nerve was impaired on the peripheral side, which may have been associated with GBS. Interestingly, the laterality of the auditory nerve impairment was marked as with other neurological signs, such as paralysis. Since fewer cases of hearing impairment associated with GBS have been reported, further neurotological approaches to GBS are necessary.

In elderly people, chronic dizziness is endemic. However, chronic dizziness of unknown origin is difficult to assess.To investigate whether mild unrecognised benign paroxysmal positional vertigo (BPPV) is a cause of isolated chronic dizziness in the elderly.The prevalence of extremely weak, horizontal, direction changing apogeotropic positional nystagmus (HAPN) that had not been detected by conventional examination was evaluated in 200 patients with isolated chronic dizziness and in 155 age matched control subjects without dizziness.A high prevalence of weak HAPN was found in patients with isolated chronic dizziness (98/200 (49.0%)) compared with the prevalence in control subjects without dizziness (25/155 (16.1%); p0.0001). Symptoms improved in some patients by daily positional exercise for BPPV.Because BPPV is the most common cause of dizziness in the elderly, and HAPN is a characteristic of horizontal canal BPPV, our findings suggest that mild persistent BPPV is a possible cause of chronic dizziness of otherwise unknown origin in the elderly.

In order to clarify vitamin E malabsorption after gastric surgery, we evaluated serum vitamin E level and neurological consequences in patients who had undergone gastrectomy for gastric cancer.We studied forty-eight patients (30 men, 18 women) with a mean age of 68.0 years, who had previously undergone gastrectomy for gastric cancer and had no evidence of recurrence. The types of operation consisted of subtotal gastrectomy in 26 patients and total gastrectomy in 22 patients. We measured postoperative body weight, white blood cells, red blood cells, hemoglobin, hematocrit, platelets, and serum levels of vitamins E, vitamin B12, folic acid, total cholesterol, triglycerides, total protein, and albumin.Serum vitamin E level was decreased in 7 (14.6%) of the 48 patients. The occurrence of low vitamin E level was significantly more frequent in the total gastrectomy group than in the subtotal gastrectomy group. In relation to reconstruction procedures, the incidence of low vitamin E level was significantly higher in patients without food passage through the duodenum. The low vitamin E level was significantly associated with low total cholesterol level. The incidence of neuropathy was significantly higher in patients with low vitamin E level.We assume that vitamin E deficiency more likely occurs after the reconstruction procedure in which food does not pass through the duodenum. Transport disturbance with loss of passage through the duodenum consequently may be the major cause of malabsorption. Differential diagnosis of neurological symptoms in post-gastrectomy patients should include hypovitaminosis E.

Jugular phlebectasia, a dilatation of the jugular veins, is a relatively rare benign condition. Although the precise etiology is unknown, an increase in intrathoracic pressure that is transmitted to the jugular vein is believed to cause the venous ectasia. However, in this case of a 70-year-old woman with right internal jugular phlebectasia, the increase in intrathoracic pressure was not transmitted to the dilated vein, although it was transmitted to the other surrounding veins. Selectively high baseline pressure in the dilated vein could have caused the venous ectasia in this case.

Prion infections lead to fatal diseases of the CNS, including Creutzfeldt-Jakob disease (CJD) in humans, bovine spongiform encephalopathy(BSE) in cows. Iatrogenic CJD which have been transmitted through dura-matter transplantation, administration of pituitary tissue extracts, corneal transplantation, or neurosurgical procedures. There are not thought to be infectious agents in blood of sporadic CJD patients. However three recipients of blood donated by individuals who subsequently developed variant CJD in United Kingdam. We introduce the guideline for CJD infection through medical procedure made in 2003 and arouse attention to risk of blood in variant CJD patients.

A 34-year-old man with MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) showed chronic intestinal pseudo-obstruction (CIPO), which was improved by the administration of distigmine bromide. He exhibited generalized tonic clonic seizures at the age of 21, and mitochondrial DNA analysis showed the MELAS mutation. At the age of 34, he became akinetic mutism after nonconvulsive status epilepticus and needed enteral nutrition through a nasogasrtic tube. However, he developed abdominal distention and vomiting, and was diagnosed as CIPO, therefore tube feeding was stopped. Although the administration of domperidone, mosapride citrate, butyric acid bacteria, sodium picosulfate, prostaglandin F2 alpha, pantothenic acid, dioctyl sodium sulfosuccinate, and so on, was ineffective, the administration of distigmine bromide improved his bowel motion disturbance and abnormal distention. The present case is the first MELAS patient with CIPO to be ameliorated by distigmine bromide, which might work acetylcholine receptor on the interstitial cells of Cajal.

Ten subjects were asked to pay attention to green or to red, when each visual stimulus was presented as two small squares, one green and the other red. They were instructed to push a button with the right hand, when the attended color was on the right side, and to push a button with the left hand, when the attended color was on the left side. The P1/N1 peak-to-peak amplitudes of visual event-related potentials were significantly higher when subjects focused attention on green rather than on red. We assume that the attended color had the effect of modulating the P1/N1 components.

T. Hirai, Y. Iguchi, M. Uchiyama, Y. Kuroiwa, I. Nakamura, S. Yokota, K. Nishioka Department of Neurology, The Jikei University School of Medicine Department of Radiology, The Jikei University School of Medicine Department of Neurology and Stroke Center, Mizonokuchi Hospital, Teikyo University School of Medicine Japan Medical Research Foundation, Yokohama City University Department of Pediatrics, Yokohama City University Institute of Medical Science, Tokyo Medical University, Japan

l -3,4-Dihydroxyphenylalanine (DOPA) is a neurotransmitter candidate. To map the DOPAergic system functionally, DOPA-induced c-Fos expression was detected under inhibition of central aromatic l -amino acid decarboxylase (AADC). In rats treated with a central AADC inhibitor, DOPA significantly increased the number of c-Fos-positive nuclei in the paraventricular nuclei (PVN) and the nucleus tractus solitarii (NTS), and showed a tendency to increase in the supraoptic nuclei (SON), but not in the striatum. On the other hand, DOPA with a peripheral AADC inhibitor elevated the level of c-Fos-positive nuclei in the four regions, suggesting that DOPA itself induces c-Fos expression in the SON, PVN and NTS. In rats treated with 6-hydroxydopamine (6-OHDA) to lesion the nigrostriatal dopamine (DA) pathway, DOPA significantly induced c-Fos expression in the four regions under the inhibition of peripheral AADC. However, under the inhibition of central AADC, DOPA did not significantly increase the number of c-Fos-positive nuclei in the four regions, suggesting that DOPA at least in part induces c-Fos expression through its conversion to DA. It was likely that the 6-OHDA lesion enhanced the response to DA, but attenuated that to DOPA itself. In conclusion, we proposed that the SON, PVN and NTS include target sites for DOPA itself.

We report a 79-year-old woman with a decreased level of consciousness. Investigation revealed an elevated serum ammonia and a portal-systemic shunt on angiography. Thus, her symptoms were thought to be due to metabolic encephalopathy. Her electroencephalogram (EEG) showed bilaterally synchronous runs of three-phase waves consistent with the triphasic waves typically seen in metabolic encephalopathy. However, after intravenous administration of diazepam, the EEG abnormalities improved; indicating that her decreased consciousness was of epileptic etiology, consistent with spike-wave stupor. Therefore, even in the presence of a clearly defined metabolic disorder, triphasic waves on the EEG may not be due to metabolic encephalopathy; they may reflect an epileptic state precipitated by the metabolic disorder.

Dominant-negative mouse prion protein (PrP) with a lysine mutation at codon 218 (Q218K) is known to inhibit prion replication. In order to gain further mechanistic insight into such dominant negative inhibition, non-glycosylphosphatidylinositol (GPI)-anchored recombinant PrP with Q218K (rPrP-Q218K) was investigated. When applied into scrapie-infected mouse neuroblastoma (ScN2a) cells, rPrP-Q218K but not wild-type rPrP (rPrP-WT) exclusively inhibited abnormal protease-resistant pathogenic isoform (PrPSc) replication without reducing the viability of the cells. It was even more efficient than quinacrine, which has already been prescribed for sporadic Creutzfeldt-Jakob disease (CJD) patients; 50% effective concentration (EC50) = 0.20 microM, 99% effective concentration (EC99) = 0.86 microM vs. EC50 = 0.45 microM, EC99 = 1.5 microM. Besides, no apparent cell damage was observed at the concentration of up to 4.3 microM (100 micrograms/ml). In combination treatment with 0.43 microM (10 micrograms/ml) of rPrP-Q218K, EC99 of quinacrine was decreased from 1.5 microM to 0.5 microM, and the cell viability was recovered from 50% to over 90% as inversely proportional to the concentration of quinacrine. Such combination could alleviate the side effects of quinacrine by reducing its effective concentration without changing or even acceleration the inhibition efficacy. Since homogeneous, high-quality rPrPs could be easily prepared from Escherichia coli in large quantities, rPrP-Q218K is a good candidate for a prion replication antagonist.

This paper reviews a variety of abnormal eye movements which include abnormal ocular positions, restricted eye motions, impairment of conjugated eye movements, abnormal smooth pursuit, abnormal saccade, gaze-evoked nystagmus, down-beat nystagmus, internuclear ophthalmoplegia, supranuclear ophthalmoplegia, square wave jerks, roving eye movement, ocular bobbing, ocular dipping, reverse ocular bobbing, and ping-pong gaze. Abnormal eye movements occur from stroke, spinocerebellar degeneration, Parkinson disease, multiple system atrophy, progressive supranuclear palsy, multiple sclerosis, Miller Fisher syndrome, myasthenia gravis, opsoclonus-polymyoclonia syndrome, and Creutzfeldt-Jakob disease. In neurological practice, it is important to observe abnormal eye movements accurately and enthusiastically, to make appropriate anatomical and etiological diagnosis.

Although mild cognitive deficits in multiple system atrophy (MSA) have been proved on neuropsychological testing, the cognitive function in MSA has not been investigated sufficiently from an electrophysiological view point. We performed a visual Event-related potential (ERP) examination and quantitative magnetic resonance imaging (MRI) measurements on 24 MSA patients and 18 normal subjects, and investigated the relationship between the ERP abnormalities and the morphological changes of the brain in MSA patients. To elicit ERPs, we used S1-S2 task which needs frontal lobe function for execution. We found significant prolongation of P3 latency and reaction time and significant attenuation of P3 amplitude in MSA, compared with normal control values. We performed the square and linear MRI measurements on MSA and normal subjects. The cerebellum, the pons, the perisylvian cerebral area and the deep cerebral gray matter in MSA were significantly smaller than those in normal subjects. The mean value in MSA was significantly increased for the bicaudate index and Huckman number compared with those in normal subjects. In MSA, we found significant correlation between P3 latency and atrophy of the cerebellum and the pons, while we found no correlation between ERP abnormalities and quantitative MRI measurements of any other regions. Our results showed that the prolongation of visual P3 latency during S1-S2 task was significantly associated with atrophy of the cerebellum and the pons.

Nerve growth factor and its receptor with tyrosine kinase activity (TrkA) have been implicated in the development of Alzheimer's disease (AD). Entire coding regions of TrkA gene harboring exons 1 through 17 were sequenced in 114 patients with sporadic AD and 112 control subjects in a Japanese population, and six known and two novel single nucleotide polymorphisms were identified, but no mutation associated with sporadic AD was identified. Concurrently, case-control analysis of TrkA gene A1674G polymorphism in 534 patients with sporadic AD and 454 control subjects has revealed no significant differences in TrkA genotype or allele frequencies even after stratification for Apolipoprotein E epsilon4 carrier statuses. Thus, the TrkA genotype does not appear to influence the risk of developing sporadic AD in a Japanese population.

To observe sensory and cognitive information processing in Parkinson's disease (PD), 34 PD patients and 26 controls were investigated. A visual oddball paradigm and an S1–S2 paradigm were employed to record the early (P1, N1, P2) and late (N2, P3) event-related potentials (ERPs) at Cz, Pz and Oz. Results showed: (1) enlarged P1 amplitude at all electrode locations on both tasks, (2) shortened N1 latency and enlarged P2 amplitude at Oz on both tasks, (3) enlarged N1 amplitude at Cz during an oddball paradigm, (4) delayed N2 latency and decreased N2, P3 amplitude on both tasks, and (5) delayed P3 latency and reaction time during the S1–S2 paradigm. Abnormal ERP changes were correlated with worsened scores on Wechsler Adult Intelligence Scale-Revised and motor dysfunction scales in PD. We surmise overactive aspects or failed inhibitory modulation of sensory information processing in the early ERP stage and deficient cognitive information processing during the late ERP stage in PD.

Visual event-related potentials (ERPs) were recorded during an oddball paradigm (OBP) and a simple reaction paradigm (SRP) to investigate the effect of stimulus-onset asynchrony (SOA) on ERPs under constant and random conditions in nine healthy individuals. NA was obtained by subtracting ERPs for SRP from those to the frequent nontarget of OBP. N2 was obtained by subtracting ERPs to the frequent nontarget from those to the rare target of OBP. N1, P2, and P3 latencies during OBP were shorter, and N1 amplitude of OBP, P1, and P2 amplitude of SRP, and NA amplitude were larger under constant conditions than under random conditions. We suggest that visual information processing is faster and more effective under constant conditions than under random conditions. NA potential related to the pattern recognition processing was significantly interfered with under random conditions, whereas N2 potential related to the stimulus classification was less influenced by the rhythm. The visual selective processing activity was influenced by the SOA with the positive shift of the waveform "20% rare target of OBP-100% target of SRP" under random conditions.

An 86-year-old woman with liver cirrhosis was admitted because of clouding of consciousness, which had been present for 3 days. She had mild fever and marked nuchal rigidity. CSF showed increased polymorphonuclear leukocytes (1620 μL), increased protein (614 mg/dL), and low glucose level (1 mg/dL). CSF culture revealed Escherichia coli …

OBJECTIVE To evaluate the influence of the age at disease onset on the clinical symptoms, laboratory findings, treatment, and complications of microscopic polyangiitis (MPA). PATIENTS From 1999 to 2001, we encountered 4 MPA patients with disease onset at age 65 or older (average 77.3, all were female: the elderly group). For comparison, 4 MPA patients with disease onset a 64 years or younger (average 44.7, two were male: the non-elderly group) were used. RESULTS There was no statistically significant difference in clinical features between the two groups. All patients in the elderly group were referred to our hospital, because of fever of unknown origin or suspicion of connective tissue disease. The elderly group had a longer duration from the first admission to the start of treatment. Renal biopsies were done in all of the non-elderly group and one of the elderly group. The diagnosis of the other 3 patients of the elderly group was based on muscle or nerve biopsy, showing necrotizing vasculitis. At the time of diagnosis, antibodies to myeloperoidase (MPO-ANCA) were positive in 7 of 8 patients (87.5%). 2 patients of the non-elderly group were died of heart failure and hepatic failure by cyclophosphamide (CYC). The other 6 patients achieved substantial improvement. CONCLUSIONS Muscle or nerve biopsy helped clinical management of elderly patients when renal biopsies could not be done. IVCY was relatively safe and effective treatment for MPA in elderly as well as non-elderly patients.

Visual event-related potentials during an oddball paradigm with movement imagery tasks were recorded in 10 right-handed subjects from 32 scalp electrodes. Rare targets and non-targets elicited early (P3e) and late (P31) P300 components. In the P3e there was no difference between the rare target and non-target. In the right-imagery task the rare target P31 amplitude was larger than the rare non-target one, whereas the rare non-target P31 amplitude was larger than the rare target one in the left-imagery task. Some of the 4 equivalent current dipole (ECD) sources were located at the subcortical regions, the cerebellum and the cingulate cortex, common to the P3e and the P31. Moreover, another P3e dipole was localized to the parietal regions, while that of the P31 dipoles to the contralateral premotor cortex. This difference between the P3e and P31 dipoles might reflect two different neural networks related with the transformation of coordinates from visual to motor space.

The convergent eye movements in convergence nystagmus are reported to be opposed adducting saccades under excessive convergence drive. What occurs is a horizontal saccade of the adducting eye and a quick reversal of the abducting eye immediately after initiation of the original saccade. Accordingly, the opposed adducting saccades of the abducting eye have been explained by the dynamic overshoot mechanism. However, by electro-oculographic analysis of eye movements in a patient with convergence nystagmus, we found that the opposed adducting saccades of the abducting eye occurred not only after but also just before initiation of the original saccade. Our observation indicates that the opposed adducting saccades can occur without dynamic overshoot as the starter mechanism. Possibly, cessation of the discharge of omnipause neurons may lead to firing of the burst neurons for the medial rectus subnucleus via activation by the excessive convergence drive.

We investigated how visual event-related potentials (ERPs) are modulated by visual divided attention using an S1-S2 paradigm. Stimulus S2 consisted of non-target stimuli (Stimulus 1, 2, 3) and a target stimulus (Stimulus 4). The spatial/color factor was compared between S1 and S2: same/same (Stimulus 1); same/different (Stimulus 2); different/same (Stimulus 3); and different/different (Stimulus 4). The P1/N1 (90 approximately 150 ms) showed significantly greater amplitude in Stimulus 3 than in Stimuli 1 and 2. The N2 (230 approximately 290ms) showed significantly greater amplitude in Stimulus 2 than in Stimuli 1 and 3. We assumed that the P1/N1 was related to spatial attention, enhanced by alterations to the spatial factor, and that the N2 was related to color attention, enhanced by alterations to the color factor.

Neuromyelitis optica (NMO) is an inflammatory disease characterized by recurrent attacks of optic neuritis and myelitis. It is generally accepted that autoantibodies against aquaporin 4 water channel protein play a pathogenic role in neuromyelitis optica. We have recently reported that plasmablasts are increased in the peripheral blood of this autoimmune disease, and are capable of producing autoantibodies against aquaporin 4. Here, we demonstrate that CD138(+)HLA-DR(+) plasmablasts, a subset of IgG-producing cells, are increased in the peripheral blood and are enriched among the cerebrospinal fluid (CSF) lymphocytes during the relapse of neuromyelitis optica. Notably, these CD138(+)HLA-DR(+) plasmablasts overexpress CXCR3, whose ligands are present in the cerebrospinal fluid during the relapse of neuromyelitis optica. These results led us to speculate that plasmablasts producing anti-aquaporin 4 autoantibodies might traffic toward the central nervous system (CNS). Furthermore, we performed single-cell sorting of plasmablasts from peripheral blood and CSF samples from NMO and sequenced the complementarity-determining regions (CDRs) of the IgG heavy chain expressed by the sorted plasmablast clones. There were high frequencies of mutations in the CDRs compared with framework regions, indicating that these plasmablast clones would represent a post-germinal center B-cell lineage. Consistent with the preceding results, the plasmablast clones from the peripheral blood shared the same CDR sequences with the clones from the CSF. These results indicate that IgG-producing plasmablasts, which are guided by helper T-cells, may migrate from the peripheral blood preferentially to the CSF. Since migratory plasmablasts could be involved in the inflammatory pathology of NMO, the B-cell subset and their migration might be an attractive therapeutic target.

To understand malalignments of the visual axes in one-and-a-half syndrome, we measured eye positions in 4 patients with this syndrome under two conditions: with Frenzel goggles to prevent eye fixation and without Frenzel goggles. When fixation was prevented with the Frenzel goggles, all patients showed mild outward deviation in both eyes. Removal of the Frenzel goggles elicited adduction of the eye ipsilateral to the side of the lesion for fixation, with greater outward deviation of the contralateral eye (acute stage), or adduction of both eyes to midposition for biocular fixation (convalescent stage). In 3 patients whose outward eye deviation with Frenzel goggles was greater on the ipsilateral side, a transition from one-and-a-half syndrome to ipsilateral internuclear ophthalmoplegia was noted, whereas a transition to ipsilateral gaze palsy was seen in the one patient whose deviation was greater on the contralateral side. These findings suggest that in one-and-a-half syndrome patients, the eyes tend to be in divergent positions when fixation is prevented; ipsilateral eye deviation may result from medial longitudinal fasciculus involvement, and contralateral eye deviation may result from paramedian pontine reticular formation involvement. Viewing a target may lead to a secondary deviation or adaptation of eye positions for fixation.

To determine whether there are characteristic changes in event-related potentials (ERPs) in parkinsonian syndromes we studied 8 patients with progressive supranuclear palsy (PSP), 10 patients with corticobasal degeneration (CBD), 9 patients with striatonigral degeneration (SND), and 16 patients with idiopathic Parkinson's disease (PD) with a mean duration of illness shorter than 5 years in each group. A visual oddball paradigm was employed to elicit P300. P300 to the rare target and rare nontarget stimuli and reaction time (RT) to rare target stimuli in each group were compared with those in the corresponding age-matched normal control group and to each other after age correction. The correlation of P300 and RT to motor disability score was also studied. In PSP P300 amplitude was markedly reduced while in CBD P300 latency was prolonged. P300 amplitude to rare nontargets in SND and PD was attenuated. The mean RT in the PSP and the CBD group was significantly longer than in the other two groups. The mean RT in PD and P300 amplitude to rare nontargets in both CBD and PD showed significant correlation with the severity of motor disability. Simultaneous measurement of P300 and RT may yield useful supplementary information in facilitating diagnosis of parkinsonian syndromes in addition to clinical criteria.

A 59 year old man with prostatic carcinoma developed epidural compression of the cauda equina caused by bony expansion from a vertebral osteoblastic metastasis. For medical reasons he could not undergo radiation or surgery. Hormonal therapy alone relieved his low back pain and restored ambulation and urinary function. Postmyelography CT showed that the bony expansion from the vertebra had completely disappeared after treatment. This is the first report of remarkable improvement due to hormonal therapy alone.

P300 was evoked by a visual oddball and an S1-S2 task in 22 non-demented Parkinson's disease (PD) patients (13 in the early stage, nine in the late stage) and 18 normal controls. Reaction time was also measured. All patients undertook the 99Tc-ECD SPECT examination. Quantitative regional cerebral blood flow (rCBF) was obtained by overlying SPECT image on the 3D-magnetic resonance image. In the PD patients in the late stage, P300 latency to S2-same and reaction time were significantly prolonged, while rCBF at bilateral frontal, temporal, and the right parietal lobes was decreased. P300 latency to S2-same was significantly correlated with the rCBF at bilateral temporal lobes. Reaction time was significantly correlated with the rCBF at the right frontal and parietal lobes, as well as the temporal and occipital lobes. The results suggest that P300 changes in non-demented PD in the late stage could be related to the temporal lobe dysfunction.

The authors monitored CSF findings for over 5 months in a patient with a fatal case of scleromyxedema and two episodes of encephalopathy. During both encephalopathy episodes, CSF protein and immunoglobulin G (IgG) levels were elevated without an increased IgG index or IgG synthesis rate. A CSF-dominant increase in the concentration of interleukin-6 (IL-6) also was noted during encephalopathy. These findings suggest a disruption of the blood-brain barrier and that IL-6 may play some role in mediating the encephalopathy. OFF

A 59 year old man had a benign scalp tumour (figure A) for over 20 years. He had not received primary immunisation against tetanus. He experienced generalised tetanus, manifested by rigidity of the masseter muscles (trismus, figure B), followed 24 hours later by …