Key words : thalamic hemorrhage, temporal change, CT scan, SEP, prognosis
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1 Key words : thalamic hemorrhage, temporal change, CT scan, SEP, prognosis
2
3 TOUCH PAIN VIBRATION POSITION OTSESTHESIA PARESTHESIA Fig. 1 Temporal changes of sensory disturbances Touch, pain, vibration and position senses show marked improvement at the follow up time (right column). But both dysesthesia and paresthesia show marked exacervation at the follow up time, though they are not severe at the onset (left column). Table 2 Incidence of SEP components in thalamic hemorrhage Although P15 component was detectable from the onset, both N20 and P23 components were rarely seen at the onset but recovered at the follow up time.
4 Normal Side Affected Side Fig. 2 Recovery of SEP components P15-N20-P23 components are seen constantly at normal side (left column). But these components are not seen at the onset but gradually become detectable at affected side (right column). Note the delay of the peak latency of P23 component. The arrows indicate the negative potential from Erb's points.
5 Table 3 Interpeak Latencies of SEP-components in Thalamic Hemorrhage Erb-P15-and P15-N20-interpeak latencies were not different between those of non affected and affected side, but N20-P23-interpeak latencies were selectively prolonged at affected side (N20/ P23 dissociation). Fig. 3 Somatosensory evoked potentials from the contralateral scalp (lower tracing) and Erb's point (upper tracing) of a patient 6 months after thalamic hemorrhage. Interpeak latencies of each component are indicated. N20-P23 interpeak latency is prolonged in recovered-sep.
6 NONAFFECTED RECOVERED Fig. 4 Distributions of interpeak latencies Interpeak latencies (msec.) of both non-affected (left) and affected (right) SEP components are plotted. Note the marked prolongation of N20-P23 interpeak latencies of recovered SEP (N20/P23 dissociation).
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8 3) Hammond EJ, Wilder BJ, Webellinger JR : Electrophysiologic recordings in patient with a discrete unilateral thalamic infarction. J Neurol Neurosurg Psychiatry 45 : , ) Maugiere F, Courjon J.: Origins of Shortlatency somatosensory evoked potentials in human. Ann Neurol 9 : 609, ) Nakanishi T, Shimada Y, Sakuta M, et al : The initial positive component of the scalprecorded somatosensory evoked potential in normal subjects and in patients with neurological disorders. Electroenceph Clin Neurophysiol 45 : 26-34, ) Noel P, Desmedt JE : Somatosensory cerebral evoked potentials after vascular lesions of the brainstem and diencephalon. Brain 98: ) Walshe TM, Davis KR, Fisher CM : Thalamic hemorrhage : A computed tomographic-clinical correlation. Neurology 27 : , ) Piepgrass U, Rieger P : Thalamic bleeding : Diagnosis, course and prognosis. Neuroradiol 22 : 85-91, ) Giblin DR : Somatosensory evoked potentials in healthy subjects and in patients with lesions of the nervous system. Ann NY Acad Sci 112 : 93, ) Shibasaki H, Yamashita Y, Tsuji S : Somatosensory criteria and abnormalities Neurol Sci 34 : , 1977 evoked potentials : Diagnostic in cerebral lesions. J 15) Tsumoto T, Hirose N, Nonaka S, et al : Cerebrovascular disease. Changes in somatosensory evoked potentials associated with unilateral lesions. Electroenceph Clin Neurophysiol 35: , ) Chiappa KH, Young RR, Goldic W : Origins of the components of human short-latency somatosensory evoked responses (SER). Neurology (NY) 29 : 598, ) Mauguiere F, Courjon J, Schott B : Dissociation of early SEP components in unilateral traumatic section of the lower medulla. Ann Neurol 13 : , ) Tsuji S, Shibasaki H, Kato M, et al : Shortlatency somatosensory evoked potentials : Their distribution and abnormalities in neurological disorders. Electroenceph Clin Neurophysiol 52 : 45, ) Cracco RQ : The initial positive potential of the human scalprecorded somatosensory evoked response. Electroenceph 32 : , 1972 Clin Neurophysiol 20) Desmedt JE, Choron G : Central somatosensory conduction in man : Neural generators and interpeak latencies of the far-field components recorded from neck and right of left scalp and
9 earlobes. Electroenceph Clin Neurophysiol 50 : 382, ) Fukushima T, Mayanagi Y, Bouchard G : Thalamic evoked potentials to somatosensory stimulation in man. Electroenceph Clin Neurophysiol 40 : , ) Celesia GG : Somatosensory evoked potentials recorded directly from human thalamus and SmI cortical area. Arch Neurol 36: , ) Chiappa KH, Choi SK, Young RR : Shortlatency somatosensory evoked potentials following median nerve stimulation in patients with neurological lesions. In Desmedt JE (eds) : Clinical uses of cerebral, brainstem and spinal somatosensory evoked potentials. Prog Clin Neurophysiol, vol 7, Kargar Barsel 1980, pp264 26) Chiappa KH, Ropper AH : Evoked potentials in clinical medicine. Part I, II. New Engl J Med 306: , ) Hume AL, Cant BR : Central somatosensory conduction after head injury. Ann Neurol 10 : , ) Carlin L, Roaeh ES, Riela A, et al : Juvenile metachromatic leukodystrophy : Evoked potentials and computed tomography. Ann Neurol 13 : , 1983 Abstract Recovery of SEP components in thalamic hemorrhages Yutaka Kudo, M.D. and Atsushi Yamadori, M.D. Department of Neurology, Hyogo Brain and Heart Center at Himeji We studied temporal change of somatosensory potentials in 24 patients with circumscribed thalamic hemorrhage. Initial clinical signs of these patients included mild ocular disturbances (anisocoria and/or conjugated deviation), contralateral hemiplegia and contralateral all modality sensory loss. With recovery these severe symptoms were replaced by dysesthesia, paresthesia and ataxia. High density area gradually blurred and finally disappeared leaving no detectable lesion by CT scan. On the contrary, SEP components which had initially disappeared reappeared gradually as clinical symptoms improved. P15 component was present in the majority of cases even at the onset of severe hemorrhage (79%). But, N20 and P23 were present only in exceptional cases with small lesions (21% and 16% respectively). P15-N20-P23 components recovered in this order. Patterns of recovery among these components were different. P15 component was seen both at the onset and at the follow up time (89%), but N20/P23 complex was not seen at the onset and seen at the follow up time (72% and 67% respectively). Thus, SEP can serve as an effective method for the evaluation of the clinical course even after thelesion becomes silent radiologically. Comparison of intact SEP and recovered SEP revealed selective prolongation of the interpeak latency between N20 and P23 in recovered SEP (p<0.01). Further, comparison of onset-sep and follow up-sep revealed (1) persistence of P15, (2) recovery of N20 with normal latency and (3) recovery of P23 with markedly prolonged latency. This N20/P23 dissociation in the later stage of thalamic hemorrhage has not been reported. Exact origin of each component of SEP following median nerve stimulation remains controversial. Ourresults support the theory that P15 originates below the thalamus, N20 originates in the thalamus and P23 originates in the thalamocortical fibers or in the primary sensory cortex. (Jpn. J. Stroke 6: , 1984)
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