LETTERS
Bilateral Sensory Seizures in a Patient with Pain Asymbolia Marcelo L. Berthier, MD," Sergio E. Starkstein, MD,*tf Martin A. Nogues, MD,*t Robert G. Robinson, MD,f and Ramon C . Leiguarda, MD' Bilateral sensory seizures (i.e., bilateral paresthesias with retained consciousness 11-21) and pain asymbolia (i.e., lack of motor and emotional reactivity to painful stimuli applied anywhere on the body surface 137) have been reported in patients with lesions involving the posterior insula and the ad jacent inner parietal operculum (second somatosensory area, SII). These disorders are quite rare and, to our knowledge, their coexistence has never been reported. A 64-year-old rght-handed man reported sensory bodily episodes that recurred up to several times daily during the previous 4 months. The spells, which lasted 60 seconds, started with sudden paresthesias in the feet that spread over the entire ventral part of the body and finished in the inferior maxilla. H e then had a feeling of tightness at the back of his throat and dysphonia, and he perceived an unpleasant odor. The seizure finished with palpitations, diaphoresis, dyspnea, and an inimse feeling of fear in the presence of clear consciousness. On neurological examination, he had mild left hemiparesis, left inferior quadrantanopia, left visual and tactile extinction, and bilateral cortical sensory loss. While sensation to pinprick, temperature, and deep pressure in the pretibial region was normally perceived on both sides, he had no motor or emotional response to painful stimuli applied anywhere on the body surface. O n psychophysiological evaluation, he showed normal pain threshold bilaterally (5 mA, 5 SD from normal control values { 31). An interictal electroencephalogram showed right
frontotemporal spikes intermixed with theta waves. A computed tomographic scan showed a right insular tumor (Fig), and a glioblastoma multiforme was found on biopsy. The patient was started on phenytoin (300 &day), which resulted in good seizure control, but the pain asymbolia remained unchanged. The insula receives bilateral sensory input and has reciprocal somatosensory connections with the amygdala [4}. Thus, our patient's bilateral sensory seizures, autonomic symptoms, and fear may have resulted from ictal discharges in the posterior insular411 region that spread via the anterior insula into the amygdala. In support of this hypothesis, similar lesions have been reported in patients with bilateral sensory seizures [1, 21, and insulotemporal hypermetabolism was the main finding in patients with lactate-induced panic attacks 151. Finally, pain asymbolia may be explained by a sensory-limbicdisconnection resulting from the extensive insular damage 131.
Institute of Neurological Research f University of Buenos Aires Buenos Aires, Argentina $Department of Psycbiatty and Behavioral Sciences Johns Hopkins University School of Medicine Baltimore, MD References 1. Lesser RP, Lueders H, Conomy JP, et al. Sensory seizure mimicking a psychogenic seizure. Neurology 1983;33:800-802 2. Young GB, Barr HWK, Blume WT. Painful epileptic seizures involving the second sensory area. Ann Neurol 1986;19:412 3. Berthier M, Starkstein S, Leiguarda R. Asymbolia for pain: a sensory-limbic disconnection syndrome. Ann Neurol 1988;24: 4 1-49 4. Mesulam MM, Mufson E. The insula of Reil in man and monkey. Architectonics, connecrivity and function. In: Peters A, Jones EG, eds. Cerebral cortex, vol4. New York: Plenum, 1985:179226 5. Reiman EM, Fusselman MJ, Fox PT, Raichle ME. Neuroanatomical correlates of anticipatory anxiety. Science 1989;243:10711074
Potential Benefits of Dopamine Striatal Implant Anthony E. Lang, MD, FRCP(C)
I was interested to read the article by During and colleagues
111 about the controlled release of dopamine from a poly-
Enhanced computed tomographic Scan showing a Large right tumor involving the entire insala.
meric brain implant. One potential use of this treatment, if such technology is eventually applied to human Parkinson's disease, relates to the selective ability of the polymeric implant to increase only striatal dopamine levels. This avoids the increase in extrastriatal dopamine concentrations which occurs with oral therapy. Psychiatric side effects of levodopa and dopamine agonists represent a common problem which is often dose limiting, particularly in the later stages of Parkinson's disease. The origin of these disturbances is not certain but may be due to stimulation of mesolimbic or
Copyright 0 1990 by the American Neurological Association
103
Bilateral Sensory Seizures in a Patient with Pain Asymbolia Marcelo L. Berthier, MD," Sergio E. Starkstein, MD,*tf Martin A. Nogues, MD,*t Robert G. Robinson, MD,f and Ramon C . Leiguarda, MD' Bilateral sensory seizures (i.e., bilateral paresthesias with retained consciousness 11-21) and pain asymbolia (i.e., lack of motor and emotional reactivity to painful stimuli applied anywhere on the body surface 137) have been reported in patients with lesions involving the posterior insula and the ad jacent inner parietal operculum (second somatosensory area, SII). These disorders are quite rare and, to our knowledge, their coexistence has never been reported. A 64-year-old rght-handed man reported sensory bodily episodes that recurred up to several times daily during the previous 4 months. The spells, which lasted 60 seconds, started with sudden paresthesias in the feet that spread over the entire ventral part of the body and finished in the inferior maxilla. H e then had a feeling of tightness at the back of his throat and dysphonia, and he perceived an unpleasant odor. The seizure finished with palpitations, diaphoresis, dyspnea, and an inimse feeling of fear in the presence of clear consciousness. On neurological examination, he had mild left hemiparesis, left inferior quadrantanopia, left visual and tactile extinction, and bilateral cortical sensory loss. While sensation to pinprick, temperature, and deep pressure in the pretibial region was normally perceived on both sides, he had no motor or emotional response to painful stimuli applied anywhere on the body surface. O n psychophysiological evaluation, he showed normal pain threshold bilaterally (5 mA, 5 SD from normal control values { 31). An interictal electroencephalogram showed right
frontotemporal spikes intermixed with theta waves. A computed tomographic scan showed a right insular tumor (Fig), and a glioblastoma multiforme was found on biopsy. The patient was started on phenytoin (300 &day), which resulted in good seizure control, but the pain asymbolia remained unchanged. The insula receives bilateral sensory input and has reciprocal somatosensory connections with the amygdala [4}. Thus, our patient's bilateral sensory seizures, autonomic symptoms, and fear may have resulted from ictal discharges in the posterior insular411 region that spread via the anterior insula into the amygdala. In support of this hypothesis, similar lesions have been reported in patients with bilateral sensory seizures [1, 21, and insulotemporal hypermetabolism was the main finding in patients with lactate-induced panic attacks 151. Finally, pain asymbolia may be explained by a sensory-limbicdisconnection resulting from the extensive insular damage 131.
Institute of Neurological Research f University of Buenos Aires Buenos Aires, Argentina $Department of Psycbiatty and Behavioral Sciences Johns Hopkins University School of Medicine Baltimore, MD References 1. Lesser RP, Lueders H, Conomy JP, et al. Sensory seizure mimicking a psychogenic seizure. Neurology 1983;33:800-802 2. Young GB, Barr HWK, Blume WT. Painful epileptic seizures involving the second sensory area. Ann Neurol 1986;19:412 3. Berthier M, Starkstein S, Leiguarda R. Asymbolia for pain: a sensory-limbic disconnection syndrome. Ann Neurol 1988;24: 4 1-49 4. Mesulam MM, Mufson E. The insula of Reil in man and monkey. Architectonics, connecrivity and function. In: Peters A, Jones EG, eds. Cerebral cortex, vol4. New York: Plenum, 1985:179226 5. Reiman EM, Fusselman MJ, Fox PT, Raichle ME. Neuroanatomical correlates of anticipatory anxiety. Science 1989;243:10711074
Potential Benefits of Dopamine Striatal Implant Anthony E. Lang, MD, FRCP(C)
I was interested to read the article by During and colleagues
111 about the controlled release of dopamine from a poly-
Enhanced computed tomographic Scan showing a Large right tumor involving the entire insala.
meric brain implant. One potential use of this treatment, if such technology is eventually applied to human Parkinson's disease, relates to the selective ability of the polymeric implant to increase only striatal dopamine levels. This avoids the increase in extrastriatal dopamine concentrations which occurs with oral therapy. Psychiatric side effects of levodopa and dopamine agonists represent a common problem which is often dose limiting, particularly in the later stages of Parkinson's disease. The origin of these disturbances is not certain but may be due to stimulation of mesolimbic or
Copyright 0 1990 by the American Neurological Association
103
