Reduction in terminal excitability of nigrostriatal dopaminergic neurons in rats following chronic L-dopa administration.

The effects of chronic L-dopa administration on antidromic excitability and the firing rate of nigrostriatal dopaminergic neurons were investigated in urethane-anesthetized rats. Rats that received daily L-dopa (100 mg/kg) and carbidopa (25 mg/kg) for 60 days showed a marked decrease in terminal excitability compared with the controls. There were no significant differences in the firing rates between the two groups. This finding may be related to impaired striatal dopamine release from exogenous L-dopa subsequent to chronic L-dopa treatment.

Are the after-effects of low-frequency rTMS on motor cortex excitability due to changes in the efficacy of cortical synapses?

OBJECTIVES: To investigate the mechanisms responsible for suppressing the amplitude of electromyogram (EMG) responses to a standard transcranial magnetic stimulus (TMS) after prior conditioning of the motor cortex with repetitive subthreshold TMS (rTMS) at a frequency of 1 Hz. METHODS: EMG responses from the first dorsal interosseous, abductor pollicis brevis and flexor carpi radialis (FCR) muscles were recorded after suprathreshold TMS of the motor cortex. In some experiments, H-reflexes were also obtained in the FCR. The amplitude of these responses was compared before and after applying from 150 to 1500 rTMS pulses to motor cortex at an intensity of 95% resting motor threshold through the same figure-of-8 coil. RESULTS: When tested with subjects relaxed, rTMS conditioning reduced the amplitude of motor evoked potentials (MEPs) to approximately 60% of pre-conditioning values for 2-10 min after the end of the conditioning train, depending on the number of pulses in the train. There was more suppression with 1500 rTMS pulses than with 150 pulses. There was no effect on H-reflexes. There was no effect on MEPs if the test stimuli were given during active contraction of the target muscle. CONCLUSIONS: The findings confirm previous observations that low-frequency, low-intensity rTMS to motor cortex can produce transient depression of MEP excitability. Since there was no effect on spinal H-reflexes, this is consistent with the idea that some of the suppression occurs because of an effect on the motor cortex itself. The lack of any conditioning effect on MEPs evoked in actively contracting muscle is not readily consistent with the idea that rTMS depresses transmission in synaptic connections to pyramidal cells activated by the test TMS pulse. An alternative explanation is that rTMS reduces the excitability of cortical neurones in relaxed subjects, so that responses to a given input are smaller than before conditioning. Voluntary contraction normalises excitability levels so that the effect is no longer seen.

Changes of middle latency somatosensory evoked potentials (SEPs) and alpha rythmicity associated with oculomotor processes.

OBJECTIVES: To evaluate median nerve somatosensory evoked potentials (SEPs) and alpha waves during different eye conditions. METHODS: Median SEPs and occipital electroencephalographs (EEG) were recorded in 6 eye conditions: eye-closed (EC), goggle (G), goggle+saccade (GS), saccade (S), eye-opened (EO) and pursuit (P), in 8 normal adults. Subjects saccaded their eyes reacting to auditory cues to watch a diode on the right or left side alternatively during the S condition, or imitated the same saccadic eye-movement as that in the S condition during the GS condition. In the P condition, subjects traced a small circle moving on a computer screen. RESULTS: Compared with the EC and G conditions, N30 (P25-N30 or P14-N30) amplitudes in C4' were significantly larger and the mean amplitude and power of the alpha band was significantly attenuated in the other 4 conditions. The amplitude and power of the alpha band differed significantly between the GS and S conditions, whereas N30 amplitudes were similar between the two conditions. N30-P45 or P45-N60 amplitudes in C4' were significantly larger in the P condition than in other conditions. CONCLUSIONS: Present findings suggest that different neural mechanisms cause alpha blocking and the modification of middle latency SEPs associated with oculomotor control.

Afferent and efferent excitabilities of the transcortical loop in patients with dentatorubral-pallidoluysian atrophy.

To evaluate the excitabilities of the transcortical loop in patients with dentatorubral-pallidoluysian atrophy (DRPLA), we studied somatosensory evoked potentials (SEPs) and evoked EMG responses (V1 and V2) in 10 patients and age-matched controls. In addition, the facilitatory effects of somatosensory inputs on motor evoked potentials (MEPs) were studied in four patients and controls. We observed attenuated or prolonged cervical and subcortical potentials and prolonged middle latency components of SEPs. The amplitudes of V2 in patients were significantly lowered compared to those in the controls, while the amplitudes and latencies of V1 were similar between the two groups. Since V2 was considered as a transcortical reflex, our results suggest reduced excitabilities of the afferent pathway of the transcortical loop in patients with DRPLA. Median nerve stimulation (MNS) 25 to 30 ms preceding transcranial magnetic stimulation (TMS) facilitated MEPs in the thenar muscle in two of the four patients and in the controls. The facilitation of MEPs by MNS tended to be independent of the reduction in V2. Such a result suggests that different neural mechanisms elicit V2 and facilitate MEPs following peripheral nerve stimulation, although further studies are needed. The combination of SEPs, evoked EMG responses and MEPs may be a useful technique to detect abnormalities of input and output coordinations of the transcortical loop.

Impaired novelty P3 potentials in multiple system atrophy--correlation with orthostatic hypotension.

Although neuropsychological tests demonstrate frontal lobe dysfunction in multiple system atrophy (MSA), assessment of frontal function using event-related brain potentials (ERPs) has not been sufficiently performed in MSA. The correlation between frontal lobe dysfunction and orthostatic hypotension (OH), which is known to cause frontal hypoperfusion, remains unclear. Our objectives were to assess frontal lobe dysfunction in MSA patients using ERPs and to elucidate the relevance of OH to changes in ERPs. Nine consecutive patients with MSA and nine age- and gender-matched healthy controls were compared by performance in the Wisconsin Card Sorting Test (WCST) and somatosensory ERPs to target and novel stimuli, namely, parietal maximal P3 (target P3) and fronto-central P3 (novelty P3), respectively. The correlation between novelty P3 and OH was evaluated in the MSA group. The MSA group showed a poorer performance in categories achieved (CA), total errors (TE) and perseverative errors by Nelson's (PEN) method in the WCST compared with the control group (CA and PEN: p<0.01; TE: p<0.02). Novelty and target P3s in the MSA group showed significantly prolonged latency (novelty: p<0.05; target: p<0.01) and reduced amplitude (novelty: p<0.02; target: p<0.01) compared with the control group. There was a significant negative correlation between novelty P3 latency and a drop in systolic blood pressure (r=0.76; p<0.02). Abnormalities of novelty P3 in the MSA group might reflect frontal lobe dysfunction, namely failure of attentional set-shifting, that was identified by the WCST. OH may play a role in the development of frontal lobe dysfunction in MSA.

The long loop reflex in spinocerebellar degeneration and motor neuron disease--its changes with TRH therapy.

This study aimed to define the characteristics of the long loop reflex (LLR) in patients with spinocerebellar degeneration (SCD) and motor neuron disease (MND), and observe changes in LLR caused by thyrotropin releasing hormone (TRH), a facilitator of cerebellar and motor neurons. The markers used for LLR were: V1-2 peak Latency (the latency between the V1 and V2 peaks); V2 peak-P24 Latency (the latency between the V2 peak and P24 of a somatosensory evoked potential); V2 Amplitude, and V2 Square (the area of the V2 wave). V1-2 peak Latency was significantly longer, and V2 Amplitude was significantly lower than the control in SCD. We attributed these alterations of the LLR to cerebellar ataxia, since all SCD cases had cerebellar ataxia, and extrapyramidal symptoms were only present in one SCD case; the MND cases with motor neuron disturbance showed no significant difference from the control. TRH injection resulted in an increase in V2 Square and a decrease in V2 peak-P24 Latency in SCD and other neurological disease patients. We regarded these changes as activation of the LLR by TRH. With TRH therapy, activation of the LLR coincided with improvement of cerebellar ataxia in SCD. Symptomatic improvement, however, was not observed and the LLR changes were not stable in MND. These results suggest that TRH-induced activation of LLR is caused by the activation of cerebellar function, and indirectly concerns with upper motor neurons because V2 Square increased in MND without pyramidal tract signs.

Electrophysiological and pharmacological studies of somatosensory reflex myoclonus.

Reflex myoclonus displays symptomatological heterogeneity involving the cortical and brain stem types that seem to originate above the spinal cord. Three cases of generalized myoclonus proved to be spontaneous and stimulus-sensitive, and increased with action. Segmental spinal myoclonus was spontaneous, stimulus-sensitive and rhythmical and decreased with action. Two cases of post-anoxic myoclonus seemed to be of the reticular reflex in which myoclonus was manifested in all muscles, particularly the proximal ones, and for which the EEG showed no spikes preceding myoclonus. The evoked electromyogram showed a long-loop reflex (LLR) of high amplitude, with no giant somatosensory evoked potential (SEP). Pharmacological examinations showed that the thyrotropin-releasing hormone (TRH) enhanced the onset of myoclonus, shortened the latency of the LLR and increased its amplitude, but caused no remarkable changes in SEP. These results indicate that TRH stimulates the medullary reticular neuron, thereby enhancing reticular reflex myoclonus. The myoclonus of a 3rd case was believed to be cortical reflex myoclonus on the basis of the emergence of giant SEP, increased LLR and the onset of spikes in the EEGs preceding myoclonic jerks, as ascertained by jerk-locked averaging analysis with muscular discharge. Pharmacologically, LLR, SEP and myoclonus showed no definite changes in response to TRH. Segmental myoclonus which seemed to have a spinal origin, showed no giant SEP, enhanced LLR or cortical spikes in the electrophysiological studies. No definite clinical or electrophysiological changes in response to TRH were observed. We believe the TRH administration test may be useful in the differential diagnosis of stimulus-sensitive myoclonus. In addition, the origins and nature of these types of reflex myoclonus are discussed.

[An assessment of dysphagia using videofluorography in Parkinson's disease and progressive supranuclear palsy].

We assessed the oropharyngeal swallowing ability in 8 patients with Parkinson's disease (PD), 8 patients with progressive supranuclear palsy (PSP), and 10 age-matched healthy controls (CTL) using videofluorography (VF). In VF studies, PD and PSP patients demonstrated food pooling on the tongue, difficulty in bolus formation, and bolus falling into pharynx before swallow. PSP patients had a significantly longer delay in the pharyngeal phase and showed food falling into larynx more often than PD patients (p < 0.05). On measurement of swallowing time periods as proposed by Robbins et al., both patient groups showed significantly longer periods during many swallowing phases (P < 0.05) compared to those in the control group, but there were no significant differences between the PD and PSP groups. However, in PSP patients, the time for "transferring the food bolus from the oral cavity to pharynx" which we defined as a distinct stage was significantly longer (p < 0.05) than that in the PD group. We think that the difference in dysphagia characteristics between the two diseases arises from the variations in pathological changes in PSP, including those in the cerebral cortex, cerebellum, pons and medulla tegmentum in addition to the basal ganglia. Dystonia in the neck muscle also plays a role in dysphagia in PSP patients. Levodopa medication, changing the form of foods and training in rehabilitation techniques such as the chin down posture, supraglottic swallowing and ice-massage of the oral region are probably effective for dysphagia in PD patients. In patients with PSP, there are few research reports about the treatment of dysphagia. However, several dysphagia treatments seem to be useful depending on the abnormal patterns in the VF. Further studies are necessary to establish more effective treatments for dysphagia in PD and PSP.

[A case of posterior cerebral artery territory infarction with micropsia as the chief complaint].

A 63-year-old man was admitted to the hospital complaining that all objects in his vision suddenly appeared small. Examination on admission revealed amnesia of recent events, recognition memory deficits, emotional disturbance, right upper quadrantanopsia and micropsia. The patient was diagnosed as posterior cerebral artery territory infarction based on brain CT scan and MRI findings which showed an ischemic lesion involving the left occipital lobe and hippocampus. We regarded the quadrantanopsia to have originated in the occipital lobe lesion and memory and emotional disturbances to have originated in the hippocampal lesion. After admission, micropsia and disturbances of memory and emotion improved within a month, but the quadrantanopsia did not recover. A comparison of the 25th and 2nd day brain CT scans indicated that the low density of the ischemic lesion near the hippocampus had become less clear and smaller. These findings suggest that the pathogenesis of micropsia in this case was a visual perceptional abnormality due to edematous change in the structures near the hippocampus. Cases of occipital artery territory infarction with micropsia, disturbances of memory and emotion, and quadrantanopsia appear to be rare, but micropsia may be overlooked since it is often masked by disturbance of memory or emotion.

[Eaton-Lambert syndrome manifested by respiratory failure associated with small cell carcinoma of the lung].

A 63-year-old man with Eaton-Lambert syndrome manifested by marked respiratory failure was reported. He began to notice blepharoptosis and diplopia in September, 1987, followed by weakness and easy fatigability in bulbar, neck and limb muscles in association with impotence by February, 1988. On admission in August, 1988, Gowers' sign, decreased tendon reflexes and muscle weakness improved by the injection of edrophonium were found. Anti-acetylcholine receptor antibody was negative. Single muscle action potential evoked in the thenar muscle was abnormally low in amplitude with the stimulation of the median nerve: repetitive nerve stimulation study revealed the waning at the low rates, but the waxing at the high rate (30 Hz), suggesting the diagnosis of Eaton-Lambert syndrome. Early gastric cancer (adenocarcinoma) was diagnosed from needle biopsy specimens in August, 1988, but no other neoplasm including thymoma or lung cancer was found. After subtotal gastric resection in September, 1988, he failed into respiratory failure, requiring artificial ventilation for seven months. Plasmapheresis and drugs such as anticholinesterase, guanidine hydrochloride, and corticosteroid were ineffective for the recovery from weakness in respiratory muscle. Lung cancer was suspected, based on a chest X-ray in March, 1989, and one month later he died of pneumonia. At autopsy, small cell carcinoma of the lung was observed, but there was neither recurrence nor metastasis of the gastric cancer. Emphasis was placed on the respiratory failure in Eaton-Lambert syndrome which has rarely been reported.

[Acute transverse myelitis associated with ECHO-25 virus infection].

A case of acute transverse myelitis associated with ECHO-25 virus infection was reported here with a brief review of the literature. The patient was a 42-year-old house wife. Without any antecedent symptoms, weakness and paresthesia of bilateral lower extremities, and sphincter disturbance developed suddenly. Neurological examination revealed paraplegia of both legs, hyperreflexia of lower extremities, bilateral positive Babinski sign and impairment of all sensory modalities below Th4 level. No abnormality was found in myelography and CT myelography. Abnormal intensity area was found in lower cervical spinal cord on MRI. Serum antibody titer to ECHO-25 virus was elevated in the convalescent stage (X4096), and 7 month later from the onset of neurological symptoms, high value was continued (X128). We diagnosed her illness as acute transverse myelitis complicating ECHO-25 virus infection. In the literature, only 3 cases of transverse myelitis following ECHO virus infection (type 2, 5, 19) were found. This case seemed to be the first case of transverse myelitis associated with ECHO-25 virus infection.

[Subacute sensory neuropathy associated with carcinoma--an autopsy case report and an analysis of Japanese cases].

A 68-year-old man was admitted to our hospital because of numbness in the hands and feet, and unsteady gait in August, 1986. On neurological examination, deep tendon reflexes were absent in all limbs without pathological reflexes. Superficial and deep sensory disturbances of a glove and stocking type up to the level of the elbow and the knee were observed. Pseudoathetosis was noted in the hands. His gait was ataxic and Romberg sign was positive. Muscle strength was slightly decreased. Sural nerve biopsy showed severe loss of large myelinated fibers. Laboratory studies for malignancy showed lung cancer (Squamous cell carcinoma). Left pneumonectomy was performed in November, 1986, but he died in March, 1987. At autopsy, neither metastasis nor direct infiltration of malignant cells in the central and peripheral nervous systems were present macroscopically and histopathologically. Degeneration of the dorsal root ganglion and the posterior columns of the spinal cord were remarkable. Since 1955, only 9 cases of subacute sensory neuropathy had been reported in Japan. We analysed 10 Japanese cases (including our case) to clarify the clinicopathological features of subacute sensory neuropathy. Clinically, ataxic gait, paresthesia, deep sensory disturbance, and depression of deep tendon reflexes were present in the majority of the cases. Neuropathologically, neuronal cell loss and degeneration of the dorsal root ganglion, posterior roots and posterior columns of the spinal cord were universal findings.

["Painful legs and moving toes" and muscle cramps spreading to the bilateral legs in a patient with alcoholic polyneuropathy].

A 37-year-old man with alcoholic polyneuropathy showed involuntary movement as intermittent flexion-extension or abduction-adduction of his toes identical to "painful legs and moving toes (PLMT)" and muscle cramps. Regarding the sequential spreading of PLMT and cramps from unilateral to contralateral leg muscles and phasic discharges observed by a needle EMG in the foot muscles during PLMT, we suppose that a spinal or supraspinal mechanism was responsible for the production of those movements. This case showed novel aspects of PLMT which was induced by sensory stimulation of the left lower leg and subsequently initiated cramps. The destruction of the lumbar sympathetic ganglion remarkably ameliorated the spontaneous PLMT and cramps, whereas sensory stimulation of the left lower leg still induced those movements. Therefore, we think that sensory inputs from peripheral nerves played a critical role in the generation of PLMT and cramps, and abnormal activities of spinal sympathetic nerves exacerbated those involuntary movements. Sensory induced PLMT may be a subgroup of this movement disorder.

[Crossed cerebello-cerebral diaschisis in olivopontocerebellar atrophy].

We reported a case of crossed cerebello-cerebral diaschisis (CCCD) in olivopontocerebellar atrophy (OPCA). A 49-year-old male was admitted with complaints of titubation, dysarthria and tremor. Examination on admission revealed exaggerated triceps, patella and achilles tendon reflexes on both sides and rigidity in left wrist. Ocular movements were slightly saccadic and speech was scanning or explosive. Finger-nose and heel-knee coordination was poor on both sides (left dominant). Cardiovascular reflex tests showed abnormal findings, suggesting insidious autonomic dysfunction. Brain CT and magnetic resonance imaging (MRI) revealed mild atrophy of the pons and cerebellum. Brain single photon emission computed tomography (SPECT) showed reduced cerebellar N-isopropyl-P-(123I) iodoamphetamine (IMP) uptake more prominent on the left than on the right side. A reduction of 123I-IMP uptake was more striking in the right thalamus, basal ganglia and frontal lobe than on the left side. The cerebellar sign which was left dominant and the left extrapyramidal sign were consistent with the side where reduction of 123I-IMP uptake was more prominent. We suggest that CCCD in our case resulted from transneuronal deactivation in the classic anatomical (cerebello-thalamo-cortical) pathway and dopaminergic (cerebello-basal ganglia-cortical) pathway. There is a possibility that CCCD reflects the development of pathological changes in OPCA.

[Event-related potentials in progressive supranuclear palsy].

Abnormal event-related potential (ERP) has been reported in several types of dementing illness including Parkinson's disease (PD) and progressive supranuclear palsy (PSP). In this paper we report the result of EPR recordings obtained in normal control subjects (14 cases) and in patients with PSP (6 cases) and PD (32 cases). ERPs were recorded from 13 scalp electrodes, using the acoustic odd-ball paradigm. All PD patients were in early stage (Yahr stage 1 to 2), and all PSP patients were in the mild-to-moderate state. In control subjects and PD patients P3 was normal. In PSP patients, only one subject (17%) showed a normal P3 component, three cases (50%) demonstrated low amplitude and normal latency P3, and two cases (33%) featured lack of normal P3 sequence. The P3 abnormalities in PSP patients were not related with dementia, but with low amplitude P3 being observed in 2 of 3 non-demented patients, and abolished P3 in a patient with only mild dementia. The result suggests that the P3 changes in PSP patients develop earlier than the cognitive dysfunction, and they are related to the underlying subcortical lesion rather than dementia.

[Decreased dopaminergic activity in hepatic encephalopathy in rats with galactosamine-induced acute liver failure].

Hepatic encephalopathy might be related to the failure of the liver to remove some toxic substances that were endogenously produced. The amino acid imbalance theory focuses on an increase of false neurotransmitters and a decrease of noradrenaline and dopamine. Therefore, we examined the activities of the dopaminergic neurons of the substantia nigra pars compacta electrophysiologically in control rats and in rats with hepatic encephalopathy induced by galactosamine. The mean firing rates of the dopaminergic neurons in rats with hepatic encephalopathy was 138.5 +/- 77.8 spikes/min. This was significantly lower than the mean value for the control rats which was 220.1 +/- 105.7 spikes/min. The terminal excitability of the dopaminergic neurons in rats with hepatic encephalopathy was also decreased significantly compared with the excitability in the control rats. Following the administration of the BCAA-rich amino acid preparation (GO-80) to rats with hepatic encephalopathy, the firing rates and the terminal excitability of the dopaminergic neurons were increased. The results of this study indicate that hepatic encephalopathy in rats with galactosamine-induced acute liver failure is associated with a decreased activity of the dopaminergic neurotransmitter system.

[Non-paralytic pontine exotropia with alternating exotropia].

We report a patient with pontine infarction who showed non-paralytic pontine exotropia (NPPE) with alternating exotropia. An 81-year old woman developed diplopia and gait disturbance. On the fourth day, she was admitted to our hospital. Oculomotor findings on admission showed that the ocular position of the left eye on forward gaze was fixed at the midline, while the right eye was abducted. When she was instructed to use the right eye for forward gaze, the left eye deviated outward. On right gaze, the left eye was not abducted and monocular nystagmus was noted in the abducted right eye. Upper gaze was limited in the right eye and convergence was not possible. The remaining ocular movements were intact. On cranial CT performed on eye closure, the left eye was abducted and the right eye was fixed at the midline. Brain MRI showed cerebral infarction located in the left paramedian portion of the middle pontine tegmentum with involvement of the medial longitudinum fasciculus (MLF) and in the ventral site of the upper pons. On the 16th day, right exotropia disappeared on eye opening without forward gaze, but forward gaze easily induced outward deviation of the right eye. On the 39th day, right exotropia on forward gaze had almost disappeared. However, left MLF syndrome and abnormal convergence were persistent when she discharged on the 76th day. In conjunction with oculomotor and neuroradiological findings, the NPPE with alternating exotropia in our patient may be due to severe MLF damage and secondary hyperactivity of the contralateral paramedian pontine reticular formation.

[Effects of novel immunosuppressant FK 506 in acute experimental allergic encephalomyelitis].

Experimental allergic encephalomyelitis (EAE) is a T cell-mediated autoimmune disease. It is widely used as an animal model of multiple sclerosis (MS). We studied the prophylactic effects of FK 506 electrophysiologically and immunohistochemically in acute EAE. Female Lewis rats were sensitized with guinea pig spinal cord in complete Freund's adjuvant. FK 506 suspended in distilled water was orally administered at 1.0, 3.2, 5.0 or 10.0 mg/kg per day for 12 successive days starting from the day of sensitization. A placebo was used as the control. Administration of FK 506 at doses of 3.2 mg/kg per day and over significantly delayed the onset of clinical signs. However, the FK 506 group showed a relapse or a chronic state following the onset of EAE. We made a time course recording of cortical somatosensory evoked potential (cortical SEP: P 15). P 15 latency in the placebo group was significantly delayed in accordance with the clinical signs and showed immediate improvement upon recovery. Prolongation of P 15 latency in the FK 506 group also occurred concomitantly with the clinical signs, but the delay continued after the loss of symptoms as well. After the onset of EAE, the infiltrating lymphocyte subset was examined by the avidin-biotin peroxidase complex (ABC) method in the lumbar spinal cord. In the placebo group, the number of OX3+ (Ia) cells and the W 3 25+: OX8+ (helper/inducer T: suppressor/cytotoxic T) ratio clearly reflected the development and remission of EAE. In the FK 506 group, however, increases in OX8+ lymphocytes were observed irrespective of clinical sign fluctuation, and there were corresponding decreases in the W 3/25+: OX8+ ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

[A case of mitochondrial encephalomyopathy with peripheral neuropathy and autonomic symptoms].

We report a 28-year-old man with mitochondrial encephalomyopathy with peripheral neuropathy and autonomic symptoms. Muscle biopsy from the quadriceps femoris muscle showed myopathic changes with ragged-red fibers and abnormal mitochondria. He experienced recurrent and acute weakness in his bilateral lower limbs. Needle electromyogram revealed neurogenic changes, and the amplitude of muscle action potential was low in the right posterior tibial nerve. Sural nerve biopsy showed a marked loss of both large and small myelinated fibers, and moderate to severe axonal degeneration was diagnosed. He experienced autonomic symptoms (nausea, constipation, hypoidosis and urinary retention) along with the weakness in his lower limbs which is considered to be a very rare situation. We hypothesized that autonomic symptoms in this case were due to the axonal degeneration that included unmyelinated fibers.

[Pure sensory stroke due to pontine lacunar infarction].

A 72-year-old woman presented a sudden onset isolated sensory deficit of medial lemniscal type in the right half of the body. MRI showed a small lacune in the left paramedian pontine tegmentum corresponding to the location of the medial lemniscus. MRI appeared to be most valuable in the topographic delineation of lacunar infarctions which were responsible for pure sensory stroke.