Cervical Cord Infarction Caused by Dissection of the Intracranial Segment of the Vertebral Artery.

Cervical cord infarction is uncommon but has been increasingly reported as a complication of vertebral artery dissection (VAD). A 54-year-old woman presented with neck pain and neurological deficit following sudden neck movement. Radiological findings suggested cervical cord infarction in the anterior spinal artery territory at the C5-C6 vertebral level and dissection of the intracranial segment of the right vertebral artery. Cervical cord infarction due to VAD is usually caused by dissection of its extracranial segment. The present case indicates that dissection of the intracranial segment of the vertebral artery can also cause cervical cord infarction.

[A case of leptomeningeal melanomatosis presenting with right abducens nerve palsy].

A 39 year-old man was admitted to this hospital because of severe headache and vomiting. He had been suffering from lumbago about one month previously, and diplopia ten days previously. The neurological examination revealed disturbance of right eye abduction, no nuchal rigidity. The cerebrospinal fluid (CSF) at the time of admission included erythrocytes (1,490/µl), white blood cell (62/µl) and increased level of protein (531 mg/dl), but no malignant cells were detected. He was treated as meningitis. Cranial magnetic resonance imaging (MRI) demonstrated heterogeneous intensity lesion in the left maxillary sinus and gadolinium enhancement of diffuse meninges and cranial nerves. Spine MRI showed gadolinium enhancement of lumbar spinal meninges and the cauda equina. Biopsy of the lesion in the left maxillary sinus was performed. The pathological findings demonstrated malignant melanoma. Because malignant cells were also observed in CSF, we diagnosed this case as leptomeningeal melanomatosis. Leptomeningeal carcinomatosis should be suspected when headache accompanied with pleomorphic clinical manifestations.

Temporal lobe epilepsy with amygdala enlargement: a morphologic and functional study.

BACKGROUND AND PURPOSE: Temporal lobe epilepsy (TLE) with nontumoral amygdala enlargement (AE) has been reported to be a possible subtype of TLE without hippocampal sclerosis (HS). The purpose of this study was to clarify morphologic and functional characteristics of TLE with AE (TLE + AE). METHODS: We evaluated gray matter volume and cerebral glucose hypometabolism using magnetic resonance imaging (MRI) voxel-based morphometry (VBM) and voxel-based statistical analysis of [(18) F]-fluorodeoxyglucose positron emission tomography (FDG-PET) images in 9 patients with TLE + AE as compared with controls. For VBM analysis, we recruited 30 age- and sex-matched healthy volunteers as controls. For the comparison of FDG-PET analysis, 9 patients with definite mesial TLE with HS (MTLE + HS), and 16 age- and sex-matched healthy controls were recruited. RESULTS: In patients with TLE + AE, a significant increase in gray matter volume was found only in the affected amygdala, and no significant decrease in gray matter volume was detected. In addition, significant glucose hypometabolism was observed in the affected amygdala, whereas significant glucose hypometabolism in the hippocampus, a prominent feature of definite MTLE+HS, was not observed. CONCLUSIONS: TLE + AE is different from MTLE + HS from morphologic and functional points of view, and the enlarged amygdala per se is potentially an epileptic focus in patients with partial epilepsy.

Role of posterior parietal cortex in reaching movements in humans: clinical implication for 'optic ataxia'.

OBJECTIVE: To clarify the spatio-temporal profile of cortical activity related to reaching movement in the posterior parietal cortex (PPC) in humans. METHODS: Four patients with intractable partial epilepsy who underwent subdural electrode implantation were studied as a part of pre-surgical evaluation. We investigated the Bereitschaftspotential (BP) associated with reaching and correlated the findings with the effect of electrical stimulation of the same cortical area. RESULTS: BPs specific for reaching, as compared with BPs for simple movements by the hand or arm contralateral to the implanted hemisphere, were recognized in all patients, mainly around the intraparietal sulcus (IPS), the superior parietal lobule (SPL) and the precuneus. BPs near the IPS had the earlier onset than BPs in the SPL. Electrical stimulation of a part of the PPC, where the reach-specific BPs were recorded, selectively impaired reaching. CONCLUSIONS: Intracranial BP recording and cortical electrical stimulation delineated human reach-related areas in the PPC. SIGNIFICANCE: The present study for the first time by direct cortical recording in humans demonstrates that parts of the cortices around the IPS and SPL play a crucial role in visually-guided reaching.

Internal structural changes in the hippocampus observed on 3-tesla MRI in patients with mesial temporal lobe epilepsy.

OBJECTIVE: Hippocampal sclerosis (HS) is observed in many intractable, mesial temporal lobe epilepsy (MTLE) patients. We aimed to delineate the internal structural changes (ISC) shown as loss of internal architecture in the hippocampus on 3-Tesla magnetic resonance imaging (3T-MRI) due to its higher spatial resolution. METHODS: We studied 12 MTLE patients who exhibited unilateral HS on conventional 1.5 Tesla-MRI. Using 3T-MRI, high resolution T2-weighted coronal images of the hippocampus were investigated by visual inspection without the use of detailed clinical information. In addition, tissue samples obtained from four patients who underwent epilepsy surgery were analyzed histopathologically. RESULTS: In addition to hippocampal atrophy (HA) in the abnormal side, blurring of the low-intensity streak, i.e., ISC, in the hippocampus was seen in 12 patients and atrophy or high signal intensity was observed in Ammon's horn or the dentate gyrus in nine patients. After four patients underwent epilepsy surgery, tissue samples showed astrogliosis and a loss of pyramidal neurons in the hippocampal body, concordant with ISC or HA on MRI examination. CONCLUSION: High-resolution MRI suggests that minute internal structural changes in the hippocampus reflect neuronal cell loss or gliosis, possibly in the early stage, and also show laterality of changes more sensitively. Different internal structural changes could further subclassify HS and may predict the surgical outcomes of seizure control based on the clinicopathological correlation.

Amygdalar enlargement in patients with temporal lobe epilepsy.

OBJECTIVE: The purpose of the study was to clarify the significance of amygdalar enlargement (AE) in patients with temporal lobe epilepsy (TLE) detected by MRI. METHODS: 11 TLE patients (eight men, mean age 45.3 (SD 18.2) years) with AE treated at Kyoto University Hospital were studied. Clinical history, ictal semiology, EEG, fluorodeoxyglucose-positron emission tomography (FDG-PET), interictal single photon emission CT (SPECT) and MRI were investigated. Amygdalar volume measured by 3 T MRI and its laterality index (LI) were compared with the three other groups: normal controls, patients with partial epilepsy of non-TLE and mesial TLE with hippocampal sclerosis (HS). RESULTS: Average age of onset was 39.8 years (SD 19.5). Eight had complex partial seizures and three had generalised seizures. Epileptiform discharges were found in the temporal area ipsilateral to the AE by EEG. Interictal FDG-PET/SPECT revealed regional hypometabolism or hypoperfusion in the ipsilateral temporal area. MRI showed AE on the right in five patients, on the left in five and bilateral in one, all without apparent HS. Ten of 11 patients were diagnosed as unilateral TLE ipsilateral to the AE by neurophysiological and neuroimaging methods. Enlarged amygdalae showed iso- to slightly high intensity in FLAIR images without enhancement. Unilateral AE was not seen in the other three groups for amygdalar volume and LI (p<0.05). DISCUSSION: AE is most likely a subtype of TLE without ipsilateral HS. This possibility of AE should be considered in TLE patients if there is no apparent HS.

Epileptic polyopia with right temporal lobe epilepsy as studied by FDG-PET and MRI: a case report.

Polyopia is one of rare, visual hallucinations. A 61-year-old man suffered from daily episodes of polyopia and generalized convulsions, and he was diagnosed as right temporal lobe epilepsy. MRI revealed right amygdalar swelling. FDG-PET showed hypometabolism in the right anterior temporal and the mesial occipital areas. Polyopia is thought to be caused by dysfunction of updating process of visual information in the visual association cortices. It was most likely that, in this patient, both mesial temporal and ipsilateral occipital areas were responsible for manifesting epileptic polyopia, as ictal onset zone and symptomatogenic zone, respectively.