PubMed · 877121
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L S Lange. 1977. Epilepsy in general practice.. https://pubmed.ncbi.nlm.nih.gov/877121/
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Polysomnography is used increasingly to investigate patients with possible sleep apnoea/hypopnoea syndrome (SAHS), but it has not been assessed critically. We thus examined prospectively the value of electrophysiological and respiratory monitoring in 200 consecutive adults (163 men, 37 women; mean [SD] age 50 [13] years) having polysomnography. At polysomnography, 91 patients had SAHS (greater than 15 apnoeas + hypopnoeas [A + H] per h asleep) and 11 had periodic limb-movement disorder. Recording sleep electrophysiologically was of no diagnostic value and SAHS could be as accurately defined by A + H per time in bed as by A + H per time asleep. 66% of patients with SAHS could be diagnosed with oximetry alone, but many of the undiagnosed patients had moderately severe SAHS and benefited from treatment. Neurophysiological sleep recording is unnecessary and oximetry alone is of limited value in the overnight investigation of patients suspected of having SAHS.
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We report a 55-year-old right-handed man with frontal lobe epilepsy manifesting recurrent speech arrest. He was known to have hypertension, hypertriglyceridemia, and gout. In the three days prior to admission, he had episodes of sudden inability to talk. These episodes lasted 10 to 30 seconds and recurred ten to twenty times a day. On admission, speech comprehension and other mental functions were normal, as were findings on neurologic examination. During the period of speech arrest, he understood spoken commands, and there was no abnormal motor activity or paresis. The episodes of speech arrest were thought to be short aphasic periods due to transient ischemic attacks in the left carotid territory. Computed tomography and magnetic resonance imaging demonstrated a small calcified lesion in the upper medial portion of the left frontal lobe. Left internal carotid angiography demonstrated no abnormal findings. After neuroradiological examination finished, he suddenly raised his right hand and followed it with his gaze and a right head turn. The EEG seizure pattern in which 20-25 Hz activity began in the left fronto-central region and spread rapidly to the right fronto-central region, which after about 8 seconds was replaced by 12-14 Hz flattening rhythmic polyspikes was detected 9 times within 60 minutes. It is most unusual for supplementary motor area seizure to present pure paroxysmal speech arrest without accompanying paroxysmal motor activity. As in our case, epileptic arrest of speech may be confused with a transient ischemic attack of the dominant hemisphere.