We studied five patients with nonhemorrhagic thalamic infarction with neuropsychological tests, CT, and somatosensory evoked responses (SERs). The three patients with left thalamic lesions had abnormalities of language, memory, visuospatial processing, intellect, and personality-changes compatible with dementia. The two patients with right thalamic lesions were not aphasic and did not have verbal memory defects, but were otherwise comparable. Four lesions occurred in the tuberothalamic artery territory and one in the deep interpeduncular artery territory. SERs revealed a delay in the first negative peak after P14 in the tuberothalamic patients, and a delay in the third negative peak (N60) in all patients.
Twenty-five patients with nonhaemorrhagic infarcts of the thalamus were studied clinically and by neuropsychological testing, computerized tomography and somatosensory evoked response (SER) recordings. Our aim was to determine whether the findings in these different tests would form distinct symptom clusters associated with different anatomical territories of the thalamus. Infarction conforming to the tuberothalamic arterial territory caused a facial paresis for emotional movements, severe neuropsychological deficits and a delay of the SER after P14. Infarction conforming to the interpeduncular profundus arterial territory caused a supranuclear vertical gaze paresis, severe neuropsychological deficits and a delay in the P60 component of the SER. Infarction conforming to the anterior choroidal territory caused a hemiparesis, moderate neuropsychological deficits and varied sensory evoked responses. Patients with infarctions conforming to the entire geniculothalamic territory had sensory loss in multiple modalities, minimal neuropsychological deficits and absence of sensory evoked responses after P14. A lacune in this territory caused pure hemisensory loss involving part of the body for the modalities of pain and light touch but not proprioception or vibration. Neuropsychological deficits were uncommon and N32 and N60 were delayed in the SER.
An accessory soleus muscle was found in the right leg of a cadaver in the dissecting room. This anomalous muscle was situated medially between the distal part of the tibia and the tendo calcaneus. The muscle arose from the anterior aponeurosis of the soleus muscle and was attached with a separate tendon to the calcaneus anteromedial to the tendo calcaneus. The soleus muscle was supplied by two nerves from the tibial nerve. The ramus posterior entered its posterior surface near the proximal border, and the ramus anterior entered the bipenniform part which was located on the anterior aspect of the soleus. One of branches from the r. anterior descended on the surface of the medial half of the bipenniform part and gave off a few twigs for this muscle part. Finally, its terminal entered the accessory soleus muscle and ramified in this muscle. In a teased preparation of the tibial nerve, both the nerve fibres composing this branch to the anomalous muscle and those constituting the r. anterior proper which supplied the bipenniform part were contained in the same funiculus. This mode of nerve supply to the soleus and the accessory soleus muscle suggested that this anomalous muscle derived from the part of the proper soleus muscle supplied by the r. anterior.
This paper describes a treatment protocol for threatened stroke in patients to carotid endarterectomy. The protocol includes the use of perioperative anticoagulation, intraoperative electroencephalographic (EEG) monitoring, and hypertension or barbiturates to protect the brain against documented ischemia intraoperatively. The rational and methods for protecting the patient from the threat of thromboembolism and cerebral ischemia during each of the periods of specific risk are discussed. The most unique feature of this protocol is the use of thiopental-induced EEG burst suppression for ischemia unresponsive to hypertension during carotid clamping, which has obviated the use of a potentially dangerous and cumbersome in-line arterial shunt.
Recording median somatosensory evoked potentials (SEPs) from scalp and neck in separate channels with the use of an ear reference, 52 patients had abnormal scalp-recorded P14 associated with normal cervical-recorded N13. The patients had multiple sclerosis or other brainstem or high cervical cord lesions. Evidence of brainstem lesions was found in 35 patients on clinical examination or by brainstem auditory evoked potentials or blink reflex. Abnormalities of P14 were correlated highly with brainstem dysfunction, but high cervical cord lesions could not be excluded by this finding. The localizing value of SEP is improved by measuring the N13 and P14 peaks separately and assessing the cervical cord-brainstem conduction time.
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