act of dressing induced the fits; no seizures were ever provoked by tactile stimulation or by any other single maneuver used during dressing. The emotional gratification of being com¬ pletely dressed could be the cause of the seizures. Fabio Cirignotta, MD Pasquale Montagna, MD Elio Lugaresi, MD Institute of Neurology University of Bologna Via Foscolo 7 40123 Bologna, Italy Laura Gervasio, MD EEG Laboratory Commune di Milano Milan, Italy 1. Woodcock HDC: A case with complete cessation of fits resembling epilepsy. Lancet 1919, p 60. Jacksonian Somatosensory Seizures as the Sole Manifestation of Chronic Subdural Hematoma paresthesias were accompanied by a sensa- tion of heaviness in the left arm, but frank weakness was denied, as was headache, visual symptoms, ataxia, or focal motor activity. The patient was unaware of antecedent trauma. Family history was unremark¬ able. Examination two weeks after the onset of symptoms disclosed no evidence of cranial injury. The patient's sensorium was clear. Functions of cranial nerves were intact. Strength, coordination, and gait were normal. All sensory modalities were preserved, including graphesthesia, stereognosis, point localization, and two-point discrimination. Muscle stretch reflexes were normal, and there were no pathologic reflexes. An interictal EEG demonstrated prominent delta activity over the right parietal region. A coronal computed tomographic scan (Figure) disclosed a right parietal chronic subdural hematoma, which was drained. Postoperatively, the patient experienced a marked reduction in the frequency of seizures. He has remained free of seizures during 12 months of treat¬ ment with phenytoin sodium. To the Editor.\p=m-\We present the first reported case, to our knowledge, in which jacksonian somatosensory sei- zures were the sole manifestation of a contralateral chronic subdural hemasomatosensory seizures resolved following evacuation of the hematoma. Report of a Case.\p=m-\Apreviously well, toma. The 43-year-old, right-handed male welder began to note transient paresthesias of the left hand, arm, and face. With each episode, which lasted from 30 to 60 s, the symptoms would spread from the distal left phalanges to include serially the entire hand, arm, shoulder, face, and torso on that side. This temporal sequence never varied. Initially occurring once or twice daily, the episodes gradually increased in frequency to ten or more per day. The Coronal section from computed tomographic scan, showing right parietal subdural hematoma and its associated contrast-enhancing membrane (arrow). Comment—Although the cardinal symptoms of chronic subdural hema¬ toma are increased intracranial pres¬ sure, alteration in mental status, and hemiparesis,12 seizures of any type are a relatively uncommon initial symp¬ tom. To our knowledge, there has been prior report of chronic subdural manifested solely by somatosensory seizures. The only prior implication of subdural hema¬ no hematoma in somatosensory seizures involved a patient in whom such sei¬ zures were only one of several mani¬ festations of the underlying hemato¬ ma.3 Notwithstanding the lack of associated neurologic signs, the pres¬ ence of somatosensory seizures proved to be of localizing value in our case. Recent reports have shown that chronic subdural hematoma may give rise to symptoms that closely simu¬ late transient ischemie attacks (TIAs).4"7 The symptoms of our patient might have been confused with recur¬ rent TIAs. The TIA-like symptoms reportedly associated with chronic subdural hematoma, however, last variably from three minutes to an hour or more, in contrast to the rela¬ tive brevity of the episodes experi¬ enced by our patient. toma Dana C. Hilt, MD Garrett E. Alexander, MD, PhD Department of Neurology Johns Hopkins University School of Medicine 600 N Wolfe St Baltimore, MD 21205 1. Cameron M: Chronic subdural hematoma: A review of 114 cases. J Neurol Neurosurg Psychi- atry 1978;41:834-839. 2. McKissock W, Richardson A, Bloom WH: Subdural hematoma: A review of 389 cases. Lancet 1960;1:1365-1369. 3. Mauguiere F, Courjon J: Somatosensory epilepsy: A review of 127 cases. Brain 1978;101:307\x=req-\ 332. 4. Melamed E, Lavy S, Reches A, et al: Chronic subdural hematoma simulating transient ischemic attacks. J Neurosurg 1975;42:101-103. 5. Welsh JE, Tyson GW, Winn HR, et al: Chronic subdural hematoma presenting as transient neurologic deficits. Stroke 1979;10:564-567. 6. Williams RS: Chronic subdural hematoma simulating transient ischemic attacks. Ann Neurol 1979;5:597. 7. Robin JJ, Maxwell JA, Pitkethly DT: Chronic subdural hematoma simulating transient ischemic attack. Ann Neurol 1978;4:154. Endocrine Dysfunction in Temporal Lobe Epilepsy To the Editor.\p=m-\Thereport by Herzog and colleagues, "Neuroendocrine Dysfunction in Temporal Lobe Epilepsy" (Archives 1982;39:133-135), offers a potential neuroendocrinologic basis for impaired fertility in epileptic women1 and the frequent occurrence of hyposexuality\p=m-\primarily erectile dysfunction\p=m-\inmen with temporal lobe epilepsy (TLE).2 We would be interested to know whether the patient who had an elevated serum prolactin level had recently experienced a seizure. Although we agree that interictal prolactin studies are normal in this clinical population, we found postictal hyperprolactinemia after complex partial seizures in all cases studied3; thus, the temporal relationship between serum prolactin determinations and the occurrence of seizures is critical. Although the clinical consequences of episodic hyper- prolactinemia are uncertain, impo- tence and decreased libido are the most common accompaniments of sus- tained hyperprolactinemia in men.4 Further studies of prolactin secretion in TLE seem warranted. Using an intravenous (IV) bolus of luteinizing hormone-releasing hormone (LH-RH) in male temporal lobe epileptics with sexual dysfunction, we found a spectrum of responses, both normal and abnormal. With a differ¬ ent technique of LH-RH infusion, Herzog et al found similar results in patients with TLE who were sexually asymptomatic. Interestingly, the mean age of Herzog's patients was 28.3 years, compared with 41.4 years for our normosexual patients with TLE and 50.0 years for those with hyposexuality. Thus, neuroendocrino¬ logic dysfunction seems to antedate overt sexual dysfunction in TLE. This conclusion may have far-reaching implications concerning aggressive medical therapy of TLE in early life and alternatives to medical therapy if those at greatest risk can be identi¬ fied. In our study, there was a positive Downloaded From: https://jamanetwork.com/ by a Auckland University of Technology User on 11/07/2020