Imre Szirmai

Strategic infarcts of the thalamus in vascular dementia.

Strategic infarcts or focal hemorrhages involving the paramedian nuclei of the thalamus may alter consciousness and produce complex neuropsychological symptoms such as impairment of memory, attention and motivation. Lesions disrupting the thalamo-prefrontal circuits lead to severe subcortical dementia. We analysed here the clinical, neuropsychological and neuroimaging data of 19 patients with cerebrovascular lesions in the thalamus. In six patients with bilateral paramedian infarcts, and in two with anterior thalamic infarcts, vascular dementia and severe personality changes developed. SPECT findings did not correlate with the neuropsychological symptoms. Transcortical sensory and motor aphasia was observed in four patients with thalamic hemorrhages and infarcts. In these patients SPECT detected hypoperfusion in adjacent cortical areas. Clinical symptoms and outcome of four patients are reported in detail. The clinico-morphological correlations of the thalamo-cortical circuits are reviewed and the possible causes of multiple cognitive and behavioural consequences of vascular thalamic lesions are discussed.

Spectral EEG analysis following hemispheric stroke: Evidences of transhemispheric diaschisis

Quantitative EEG frequency analysis was performed within the acute stage and after the recovery in 40 patients with hemispheric stroke in order to analyze ipsi‐ and contralateral alpha peak frequency (APF) and band power changes. Localization of hemispheric lesion was determined by computer tomography. Changes of clinical scores were compared with the alpha asymmetries. In the cases of small subcortical infarcts good improvement of alpha activity was observed over the affected hemisphere; contralateral APF was relatively preserved. Bilateral symmetric reduction of APF was found in territorial middle cerebral artery infarcts, with poor tendency of recovery of alpha power and neurologic status. These findings suggest transitory derangement of alpha generators in the contralateral hemisphere evidenced by APF and power asymmetries. EEG signs of contralateral alpha reduction may be due to the remote effect of primary ischemic lesion indicating an electrical diaschisis phenomenon in the acute phase of stroke. EEG signs of diaschisis may anticipate a poor recovery of alpha activity and clinical status in the post‐stroke period.

Impaired rhythm generation in essential tremor

It has been suggested that the cerebellum plays a role in the event‐based timing of synchronized repetitive movements. We hypothesized that regularity of rhythmic movements in essential tremor (ET) is impaired, since several lines of evidence suggest the involvement of the cerebellum in the pathomechanism of ET. To test this assumption, we examined the regularity and the maximum frequency of auditory paced repetitive movements at slow and fast stimulus rate in 34 ET patients. Variability of rhythmic finger tapping and alternating hand movements, defined by the standard deviation of movement offset before or after the pacing signal, was significantly higher compared to healthy controls. Timing of rhythmic movements of the two hands was disturbed to the same degree. Our results suggest a severe deficit of event‐based rhythm generation on both sides in ET, supporting the presumed bilateral cerebellar dysfunction in this disorder.

MR findings in subacute combined degeneration of the spinal cord caused by nitrous oxide anaesthesia – two cases

Vitamin B12 deficiency causes haematological and neurological diseases. Subacute combined degeneration (SCD) of the spinal cord is characterized by degeneration of the posterior and lateral columns.

Superior sensitivity of motor over somatosensory evoked potentials in the diagnosis of cervical spondylotic myelopathy

Myelopathy secondary to cervical spondylosis is often a difficult clinical diagnosis. Furthermore, with the introduction of magnetic resonance imaging (MRI) an increasing number of patients are identified with spondylotic cervical spinal cord compression. We analyzed the value of functional assessment of the spinal cord by motor and sensory evoked potentials (MEP and SEP) in the detection of myelopathy, with special emphasis on the correlation of clinical and electrophysiological findings. Fifty‐one patients with at least some degree of spinal cord compression because of cervical spondylosis, as shown by MRI, were included in the study, grouped according to clinical symptoms. We found that patients who had no clinical symptoms whatsoever indicating myelopathy (they were referred to MRI examination mostly because of cervical radiculopathy), had in the large majority normal MEP and SEP findings. Patients with slight, unspecific and non‐confirmative symptoms without pyramidal signs had mostly abnormal MEP but normal SEP findings. This points to the superior sensitivity of MEP over SEP in detecting myelopathy in its early stages. Patients with obvious clinical signs of myelopathy, including pyramidal signs had both abnormal MEP and SEP findings. Altogether these findings may help clinicians in interpreting MRI signs of cervical spinal cord compression.

Reversible focal MRI abnormalities due to status epilepticus : an EEG, single photon emission computed tomography, transcranial Doppler follow-up study

We demonstrate clinical data and findings of MRI, transcranial Doppler (TCD), single photon emission computed tomography (SPECT) and electroencephalography (EEG) in an 8 month follow-up study of a 15 year old girl who developed focal status epilepticus with sensory and visual illusions. EEG showed right temporal and occipital seizure activity and attenuation of the alpha activity with right predominance. MRI showed a right temporo-parietal hyper signal on the T2 weighted images involving the cortex with sulcal effacement. MRI-angiography suggested insufficient flow in the right transverse sinus. TCD detected an elevated flow velocity in the ipsilateral middle cerebral artery during status epilepticus, corresponding to an increased perfusion of the epileptic area revealed by SPECT. After normalization of the TCD finding, the MRI detected persistent cortical abnormality beyond the 70th day after admission. MRI normalized on the 103rd day of follow-up. Serial EEG frequency analysis demonstrated the recovery of alpha peak frequency on the left side, but the attenuation of rhythmic signals remained persistent on the right. In our case, the restitution of postictal EEG lag behind the consolidation of MRI signal abnormality.

Reversible nerve conduction slowing in hyponatremia

Sirs: The best known neurological complications of systemic hyponatremia are disorders of central nervous system function, such as encephalopathy and central pontine myelinolysis [1, 4, 5]. Its effect on peripheral nerve function is less well known. We present a patient who underwent nerve conduction studies before and after the correction of severe hyponatremia. The female patient of 71 years of age had a history of hypertension and trigeminal neuralgia, and was receiving diuretic and carbamazepine treatment. About a year before admission she began to complain of paresthesia and involuntary jerking in her legs, unstable gait, dizziness and headache. These complaints together with the findings of neurological examination (brisk tendon reflexes, pyramidal signs, distal sensory disturbance and spinal ataxia) were suggestive of an encephalo-myelopathy. MRI of the spine and brain was uninformative, CSF and vitamin B12 levels were likewise normal. The sodium level on admission was slightly reduced (131 mmol/l; norm. range 135–148 mmol/l); previous laboratory tests also showed consistently lower sodium levels. Chronic hyponatremic encephalo-myelopathy, brought on by the combined effect of diuretic and carbamazepine treatment, was therefore proposed as an explanation for the clinical picture. Meanwhile, during the course of her stay in the hospital she acquired a gastrointestinal infection causing vomiting for several days. During this time the patient became somnolent, confused and EEG showed diffuse slowing. Laboratory testing revealed severe hyponatremia (105 mmol/l), with normal potassium and calcium levels. This confirmed the diagnosis of acute hyponatremic encephalopathy, as a result of further gastrointestinal loss of sodium. The gradual correction of sodium levels resulted in almost full recovery, even the neurological signs seen at initial presentation showed improvement. During the stage of severe hyponatremia nerve conduction studies were performed by one of the authors (Zs. A.); the results are summarized in Table 1. Moderate conduction slowing was observed in all the nerves examined, without temporal dispersion or conduction blocks. F wave persistence was normal. One week later, after sodium levels reached 135 mmol/l and the patient had improved substantially, nerve conduction studies were repeated. This time all conduction velocities and F wave minimum latencies were within normal limits (Fig. 1). The difference in conduction velocities and F wave minimum latencies between the two examinations was about 12–30 % or 10–15 m/s, being more conspicuous in longer nerve segments. Our case study demonstrates that severe systemic hyponatremia in addition to central nervous system dysfunction may cause moderate uniform slowing of peripheral nerve conduction velocity as well, which is promptly restored to normal upon correction of the hyponatremia. There have been so far LETTER TO THE EDITORS

Impairment of post-movement beta synchronisation in parkinson's disease is related to laterality of tremor

OBJECTIVE Post-movement beta synchronisation (PMBS) is a physiological indicator of the activity of movement related neural networks. To investigate the pathophysiology of this phenomenon, we examined its characteristics in patients with unilateral tremor-dominant Parkinsons disease (PD). METHODS Movement duration and PMBS was measured after self-paced movement of the thumb at movement-reactive beta frequencies, over the supplementary motor area in 10 PD patients and 8 control subjects. RESULTS Movement duration in PD patients was longer than in controls. In left hand tremor patients, movement of the left hand was significantly longer compared to the right hand. When PD patients moved their non-affected hand, similarly to the controls, PMBS was higher contralateral to the movement. After movement of the tremulous hand, the contralateral PMBS decreased significantly and the contralateral preponderance disappeared. In the same hemisphere, PMBS was higher after contralateral to the non-affected hand movement, than after ipsilateral to the tremulous hand after movement. CONCLUSIONS PMBS in PD is affected by the activity of tremor related neural networks, suggesting that both cortical and subcortical sources are responsible for its generation. Examination of PMBS in various neurological diseases might provide further data on its physiological significance.

Vogt-Koyanagi-Harada disease presenting initially as aseptic meningoencephalitis.

Vogt–Koyanagi–Harada (VKH) disease in a Gypsy woman was diagnosed 4 months after her initial complaints. The delay is explained by the facts that: (1) the characteristic ophthalmological symptoms, which usually herald the disease and ensure early diagnosis, developed only late during the course; and (2) only retrospective analysis of the cerebrospinal fluid (CSF) cell preparation proved the presence of melanin‐laden macrophages (MLMs), specific for the syndrome.

Cortical auditory disorder caused by bilateral strategic cerebral bleedings. Analysis of two cases

The authors present the anatomical and clinical features of cortical auditory dysfunction in two patients, in whom hypertensive bleedings destroyed the cortical auditory centres in both hemispheres. The second haemorrhage occurred four years after the first bleeding in both cases. The bleedings isolated the cortical hearing centres due to the destruction of the right and left temporal white matter. During the clinical course the symptomatology has changed in both patients: pure word deafness has transformed to cortical deafness and generalised auditory agnosia. Normal pattern of brain stem auditory evoked potentials suggested intact auditory pathways. Authors conclude that transformation of clinical forms of cortical auditory disorder can be explained by the tissue reaction to the subcortical bleeding in the cortical auditory centres.