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Presence or absence of awareness in homonymous hemianopia
Six out of 7 patients having a parietal lesion had abnormal responses to stimuli contralateral to the lesion: D, was increased in 4 patients and in 2 patients there was no correlation between A and D. (Fig. 1) Three patients having a frontal lesion had normal responses to both sides. D, was equal for
responses to PUR and PUL. The abnormalities encountered in patients with a parietal lesion might be explained by 3 possible mechanisms: 1. Slight, undetected hemianopic field defects. 2. Hemi-inattention. 3. A disturbance in the computation of saccadic amplitudes.
Presence or absence of awareness in homonymous hemianopia. P.J. Koehler, (The Hague)
L.J. Endtz,
and J. te Velde
In patients suffering from liemianopia a number is consciously affected while others are unaware of any visual defect. Differences in localisation of the underlying lesions have been advanced by a number of authors, but the supporting data are generally insufficient and the conclusions contradictory. In the present study concerning 38 patients the extent of the lesions was measured on CT-scans. The centre of each lesion and its relative position was calculated in five planes with a
computer program. Unawareness of homonymous hemianopia was associated with more extensive and more anteriorly situated lesions (occipitoparietal occipitotemporal and regions). awareness of Partial and complete homonymous hemianopia was associated with pure occipital lesions. Unawareness of homonymous hemianopia may be caused by a parietal lesion or by an interruption of the associative pathways to the primary or secondary associative visual cortex in the occipitoparietal or occipitotemporal region.
The visual blink reflex in patients with encephalopathy. D.L.J. Tavy, H.H.E. MorrC, and T.C.A.M. van Woerkom (The Hague) We studied the visual blink reflex (VBR) and the orbicularis oculi reflex (OOR) in patients with diffuse encephalopathy. Twelve patients had a toxic-metabolic encephalopathy, 2 patients had an obstructive hydrocephalus and 1 patient had suffered a head injury. In each case an EEG was made. No clinical or radiological (CT-scan) evidence of structural brain stem pathology was found. Light flashes were used to evoke the VBR, while the OOR was elicited by percutaneous electrical stimulation at the site of the supraorbital foramen. The reflex contraction of the orbicularis oculi muscles was recorded with surface electrodes placed on the lower eyelids. Fifteen, healthy, age matched, subjects were used as controls. In these controls, the mean latency of the VBR was 48 f 5.0 ms for each eye. Mean latencies of the Rl and R2 were respectively
10.6 + 1.25 ms and 32.0 + 5.5 ms. In 12 patients an abnormal VBR, consisting of a symmetrically increased latency time, was found. Mean latencies of the VBR in the patient group were 111 + 28 ms. The other 3 patients did not show a VBR at all. After recovery, 2 patients showed a normal VBR, while in the third patient still no VBR could be elicited. Because in some healthy subjects the VBR can be absent, the VBR of this last patient could not be considered abnormal. So we concluded that the VBR was abnormal in 14 of the 15 patients. Testing of the OOR showed 1 patient with abnormal Rl responses, next to absent R2 responses. Further more, in 7 cases R2 responses with abnormally increased latencies were found. The mean latency of the Rl responses was 11.9 f 2.2 ms, while the R2 responses had a mean latency of 38.8 -t 7.5 ms. It appears from this study that in diffuse encephalopathy, not only the OOR can be disturbed, but that the VBR can be altered as 225
responses to PUR and PUL. The abnormalities encountered in patients with a parietal lesion might be explained by 3 possible mechanisms: 1. Slight, undetected hemianopic field defects. 2. Hemi-inattention. 3. A disturbance in the computation of saccadic amplitudes.
Presence or absence of awareness in homonymous hemianopia. P.J. Koehler, (The Hague)
L.J. Endtz,
and J. te Velde
In patients suffering from liemianopia a number is consciously affected while others are unaware of any visual defect. Differences in localisation of the underlying lesions have been advanced by a number of authors, but the supporting data are generally insufficient and the conclusions contradictory. In the present study concerning 38 patients the extent of the lesions was measured on CT-scans. The centre of each lesion and its relative position was calculated in five planes with a
computer program. Unawareness of homonymous hemianopia was associated with more extensive and more anteriorly situated lesions (occipitoparietal occipitotemporal and regions). awareness of Partial and complete homonymous hemianopia was associated with pure occipital lesions. Unawareness of homonymous hemianopia may be caused by a parietal lesion or by an interruption of the associative pathways to the primary or secondary associative visual cortex in the occipitoparietal or occipitotemporal region.
The visual blink reflex in patients with encephalopathy. D.L.J. Tavy, H.H.E. MorrC, and T.C.A.M. van Woerkom (The Hague) We studied the visual blink reflex (VBR) and the orbicularis oculi reflex (OOR) in patients with diffuse encephalopathy. Twelve patients had a toxic-metabolic encephalopathy, 2 patients had an obstructive hydrocephalus and 1 patient had suffered a head injury. In each case an EEG was made. No clinical or radiological (CT-scan) evidence of structural brain stem pathology was found. Light flashes were used to evoke the VBR, while the OOR was elicited by percutaneous electrical stimulation at the site of the supraorbital foramen. The reflex contraction of the orbicularis oculi muscles was recorded with surface electrodes placed on the lower eyelids. Fifteen, healthy, age matched, subjects were used as controls. In these controls, the mean latency of the VBR was 48 f 5.0 ms for each eye. Mean latencies of the Rl and R2 were respectively
10.6 + 1.25 ms and 32.0 + 5.5 ms. In 12 patients an abnormal VBR, consisting of a symmetrically increased latency time, was found. Mean latencies of the VBR in the patient group were 111 + 28 ms. The other 3 patients did not show a VBR at all. After recovery, 2 patients showed a normal VBR, while in the third patient still no VBR could be elicited. Because in some healthy subjects the VBR can be absent, the VBR of this last patient could not be considered abnormal. So we concluded that the VBR was abnormal in 14 of the 15 patients. Testing of the OOR showed 1 patient with abnormal Rl responses, next to absent R2 responses. Further more, in 7 cases R2 responses with abnormally increased latencies were found. The mean latency of the Rl responses was 11.9 f 2.2 ms, while the R2 responses had a mean latency of 38.8 -t 7.5 ms. It appears from this study that in diffuse encephalopathy, not only the OOR can be disturbed, but that the VBR can be altered as 225