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Sympathetic storms in a child with a midbrain glioma: a variant of diencephalic seizures
Sympathetic Storms in a Child With a Midbrain Glioma: A Variant of Diencephalic Seizures Keith Y.C. Goh, MBBS*, Edward J. Conway, MD†, Robert C. DaRosso, MD†, Cheryl A. Muszynski, MD†, and Fred J. Epstein, MD†
Introduction The term diencephalic seizures or diencephalic epilepsy was adopted to describe episodes of sympathetic nervous system hyperactivity observed and reported in several patients from as early as 1929 [1]. These episodes were attributed to disruption of the diencephalon from causes such as tumor, hydrocephalus, or trauma [2-4]. However, this clinical entity is not well understood, and there has been a paucity in published reports regarding treatment options and pathophysiology. In this report the authors describe a 7-year-old child, one of the youngest patients reported to date, who developed repeated episodes of sympathetic hyperactivity after surgical resection of a midbrain pilocystic astrocytoma and was successfully treated with clonidine. The present state of knowledge in published reports is also reviewed.
Case Report
The authors report the unusual case of a 7-year-old child, one of the youngest reported to date, who developed repeated episodes of sympathetic hyperactivity after surgical resection of a midbrain glioma. These paroxysmal events were similar to previously described diencephalic seizures. However, there was no evidence of epileptogenic activity on electroencephalography, and radiologic imaging did not reveal hydrocephalus or intraparenchymal hemorrhage. In this report, clinical features are described of this patient, along with the novel use of clonidine—a sympathetic blocking agent—in his treatment, published reports are reviewed on diencephalic seizures, and steps are recommended in the treatment of a patient who presents in this manner. The authors believe that diencephalic seizures can present with a spectrum of autonomic features, and treatment should be tailored with the appropriate pharmacologic blockade. © 1999 by Elsevier Science Inc. All rights reserved. Goh KYC, Conway EJ, DaRosso RC, Muszynski CA, Epstein FJ. Sympathetic storms in a child with a midbrain glioma: A variant of diencephalic seizures. Pediatr Neurol 1999;21:742-744.
From the *Pediatric Neurosurgery Unit; KK Women’s and Children’s Hospital; Singapore; and †Department of Pediatric Neurosurgery and Pediatric Critical Care Unit; Institute for Neurology and Neurosurgery; Beth Israel Medical Center (North Division); New York, New York.
742
PEDIATRIC NEUROLOGY
Vol. 21 No. 4
A 7-year-old male was referred for progressive headache associated with left hemiparesis and left facial palsy. Magnetic resonance imaging of the brain revealed the presence of a large tumor involving the midbrain and thalamus on the right (Fig 1). He underwent an image-guided (Viewing Wand, Elekta, Crawley, United Kingdom) craniotomy and partial surgical resection of the tumor (histologic finding of pilocytic astrocytoma). In the postoperative period, he had increased neurologic deficits, namely bilateral third nerve palsies, left facial nerve palsy, and spastic quadriparesis, which was worse on the left side. Within the first postoperative week, he began developing repeated episodes of tachycardia (150-180 bpm), hypertension (180/120 mm Hg), fever (38.4-39.5°C), sweating, muscle spasms, decorticate posturing, nystagmus, and teeth grinding. During these episodes, his oxygen saturation remained at 100%. An electroencephalogram (EEG) was performed that revealed diffuse slow-wave activity but no evidence of an epileptogenic focus. A computed tomography scan revealed no hydrocephalus or intraparenchymal hematoma. After a presumptive diagnosis of seizures, phenytoin was initiated and maintained at therapeutic levels with 100 mg twice daily. However, the episodes persisted, with frequencies of 4-6 times daily, and could only be controlled with benzodiazepines (Valium 1 mg every 6 hours or Ativan 1 mg intravenously as needed). The clinical impression was that these seizurelike episodes were periods of intense sympathetic hyperactivity, and clonidine was initiated at an initial dosage of 50 g every 12 hours. This dosage was increased eventually to 100 g every 8 hours after a good clinical response, and control of these episodes was achieved. The benzodiazepines were discontinued but phenytoin was maintained at 100 mg twice daily. The child continued to recover neurologically and was eventually sent for radiation therapy of his residual tumor. At 6 months follow-up, he had no tumor progression, phenytoin and clonidine were discontinued, and no further episodes occurred.
Communications should be addressed to: Dr. Goh; Pediatric Neurosurgery Unit; KK Women’s and Children’s Hospital; 100 Bukit Timah Road; Singapore 229 899. Received March 25, 1999; accepted June 2, 1999.
© 1999 by Elsevier Science Inc. All rights reserved. PII S0887-8994(99)00069-7 ● 0887-8994/99/$20.00
Figure 1. Axial T1-weighted magnetic resonance image (with contrast) (TR ⫽ 10,002, TE ⫽ 152/Ef) revealing the brightly enhancing lesion in the midbrain after partial surgical resection.
Discussion The term diencephalic seizures was first coined by Penfield [1] in 1929 to describe an atypical and uncommon form of what he thought was seizure activity in a patient with a tumor of the dorsal medial nucleus of the thalamus. In his patient, periodic episodes of headache, hypertension, vasodilatory changes in the skin, shivering, lacrimation, and pupillary change occurred, and eventually Cheyne-Stokes respiration and death. In 1934, 1945, and 1973, three patients with tumors involving the hypothalamus, thalamus, or hypothalamic-thalamic-third ventricle were reported as having such repeated autonomic episodes [2,5,6]. In 1987, Bullard [4] described two patients with severe diffuse head injury who developed episodes of increased temperature, respiratory rate, pulse, and blood pressure, diaphoresis, and extensor posturing. The computed tomography scans revealed no focal injury and EEGs again revealed only severe slowing. In 1988, Talman et al. [3] then reported two additional patients with similar autonomic episodes, this time with acute hydrocephalus. After shunting procedures were performed, the symptoms completely resolved without requiring medication. The most recently reported case was in 1998 from Boeve et al. [7], who described a 17-year-old female with a traumatic left temporal contusion and subarachnoid hemorrhage. The paroxysmal sympathetic storms in this patient were successfully treated with morphine sulphate. Typically, these episodes are characterized by changes in autonomic activity (i.e., body temperature, blood pressure, heart and respiratory rate, pupillary size, and sometimes hyperhidrosis, diaphoresis, and abnormal posturing, all of which occur in a paroxysmal fashion). Although sympathetic hyperactivity seems to predominate, episodes of hypothermia and bradycardia can occur as well, partic-
ularly when the etiology is related to congenital maldevelopment, such as in agenesis of the corpus callosum [8-12]. Other reported etiologies include tumors in the region of the thalamus and hypothalamus, head trauma, and acute hydrocephalus (Table 1). What is the underlying pathophysiology of these autonomic episodes? The original hypothesis was that these attacks were a form of epileptic activity, with the diencephalon implicated as the site at which damage led to seizurelike activity [1,2,5,6]. However, because no evidence for an epileptogenic focus has ever been demonstrated by EEG even during these episodes, and because most patients do not benefit from antiepileptic therapy, the term seizure is clearly a misnomer [4,8,11]. A review of all previously reported cases revealed evidence of either hydrocephalus or a lesion in the region of the brainstem or diencephalon. It has been suggested that ventricular dilatation, with subsequent rostral-caudal transtentorial herniation and brainstem compression, may lead to the intraventricular release of neuropeptides, inhibition of agents, such as endorphins, or the disruption of dopamine transmission from stretching of striatal dopaminergic fibers, thus resulting in disordered autonomic activity [3]. In one reported case, dilatation of the third ventricle caused medial hypothalamic dysfunction, which resolved after shunting [13]. Similarly, in the three patients with severe head trauma, it is possible that intermittent hydrocephalus or fluctuations in intracranial pressure may have contributed to the episodic signs. In the case of tumors that are present in the region of the diencephalon the pathophysiology is most likely an activation or a disinhibition of the central sympathoexcitatory regions, such as the paraventricular hypothalamic nucleus, lateral periaqueductal gray substance, or rostral ventrolateral medulla. Sympathetic excitation has been demon-
Goh et al: Sympathetic Diencephalic Seizures 743
Table 1.
Review of cases with automatic sympathetic seizures
Author
Patients (n)
Age (yr)
Penfield [1]
1
41
MacLean [5]
1
38
Engle and Aring [6] Solomon [2]
1 1
17 1
Bullard [4]
2
24; 24
Talman et al. [3]
2
26; 29
Boeve et al. [7]
1
17
Pathologic Findings Tumor: cholesteatoma left thalamus Tumor: astroblastoma hypothalamus Tumor: cyst left thalamus Tumor: astroblastoma hypothalamus and left thalamus Trauma: diffuse head injury (two patients) Acute hydrocephalus (two patients) Trauma: left temporal contusion
strated to occur in experimental neurogenic hypertension in which there are lesions in the hypothalamus or medulla [14]. Furthermore, activation of somatosympathetic spinal or medullary reflexes, which are triggered from muscle mechanoreceptors and chemoreceptors during episodes of hypertonia, likely have a contributory role as well [7]. It is important, therefore, to recognize the clinical features of these autonomic episodes and to treat them in an appropriate fashion. In this patient the sympathetic storms necessitated some form of blockade or suppression. Morphine sulphate and bromocriptine have been used successfully before. The mode of action is presumably from the peripheral suppressive effects of the opioids on somatosympathetic or vagal afferents and from modulation of dopaminergic pathways [4,7]. The choice of clonidine, which is an ␣-adrenergic agent used in the treatment of hypertension, was based on its action of stimulating the ␣-2-adrenoceptors in the brainstem, thus activating inhibitory neurons. The sympathetic outflow is reduced, leading to a drop in heart rate and reduced vasomotor tone. From this review, episodic autonomic dysfunction clearly occurs with variation in clinical features and secondary to various etiologies. The most important step in treating these patients is to first exclude a surgically treatable cause, such as hydrocephalus, that requires shunting, a tumor that requires resection, or a traumatic contusion or hematoma that should be evacuated. After excluding such causes the most appropriate pharmacologic intervention should be attempted to abolish these attacks.
744
PEDIATRIC NEUROLOGY
Vol. 21 No. 4
Medication
Outcome
Nil
Death
Nil
Death
Nil Phenytoin ⫹ primidone
Death Well controlled with both drugs
Morphine ⫹ bromocriptine Nil
Medication discontinued in one patient at 3 mo Resolution with ventriculoperitoneal shunting Medication discontinued at 3 mo
Morphine
References [1] Penfield W. Diencephalic autonomic epilepsy. Arch Neurol Psychiatry 1929;22:358-74. [2] Solomon GE. Diencephalic autonomic epilepsy caused by a neoplasm. J Pediatr 1973;83:277-80. [3] Talman WT, Florek G, Bullard DE. A hyperthermic syndrome in two subjects with acute hydrocephalus. Arch Neurol 1988;45:1037-40. [4] Bullard DE. Diencephalic seizures: Responsiveness to bromocriptine and morphine. Ann Neurol 1987;21:609-11. [5] McLean AJ. Autonomic epilepsy: Report of a case with observation at necropsy. Arch Neurol Psychiatry 1934;32:189. [6] Engle GL, Aring CD. Hypothalamic attacks with thalamic lesion. I. Physiologic and psychologic considerations. II. Anatomic considerations. Arch Neurol Psychiatry 1945;54:37-44. [7] Boeve BF, Wijdicks EFM, Benarroch EE, Schmidt KD. Paroxysmal sympathetic storms (diencephalic seizures) after severe diffuse axonal head injury. Mayo Clin Proc 1998;73:148-52. [8] Shapiro WR, Williams GH, Plum F. Spontaneous recurrent hypothermia accompanying agenesis of the corpus callosum. Brain 1969;92:423-36. [9] LeWitt PA, Newman RP, Greenberg HS, Rocher LL, Caine DB, Ehrenkranz JR. Episodic hyperhidrosis, hypothermia and agenesis of the corpus callosum. Neurology 1983;33:1122-9. [10] Carr-Locke D, Millac P. Diencephalic epilepsy in a patient with agenesis of the corpus callosum confirmed by computerised axial tomography. J Neurol Neurosurg Psychiatry 1977;40:808-14. [11] Summers GD, Young AC, Little RA, Stoner HB, Forbes WS, Jones RA. Spontaneous periodic hypothermia with lipoma of the corpus callosum. J Neurol Neurosurg Psychiatry 1981;44:1094-9. [12] Fox RH, Wilkins DC, Bell JA, et al. Spontaneous periodic hypothermia: Diencephalic epilepsy. BMJ 1973;2:693-5. [13] Darnell RB, Arbit E. Reversible diencephalic dysfunction: Episodic hyperhidrosis due to a trapped third ventricle. Neurology 1993;43:579-82. [14] Talman WT. Cardiovascular regulation and lesions of the central nervous system. Ann Neurol 1985;18:1-13.
Introduction The term diencephalic seizures or diencephalic epilepsy was adopted to describe episodes of sympathetic nervous system hyperactivity observed and reported in several patients from as early as 1929 [1]. These episodes were attributed to disruption of the diencephalon from causes such as tumor, hydrocephalus, or trauma [2-4]. However, this clinical entity is not well understood, and there has been a paucity in published reports regarding treatment options and pathophysiology. In this report the authors describe a 7-year-old child, one of the youngest patients reported to date, who developed repeated episodes of sympathetic hyperactivity after surgical resection of a midbrain pilocystic astrocytoma and was successfully treated with clonidine. The present state of knowledge in published reports is also reviewed.
Case Report
The authors report the unusual case of a 7-year-old child, one of the youngest reported to date, who developed repeated episodes of sympathetic hyperactivity after surgical resection of a midbrain glioma. These paroxysmal events were similar to previously described diencephalic seizures. However, there was no evidence of epileptogenic activity on electroencephalography, and radiologic imaging did not reveal hydrocephalus or intraparenchymal hemorrhage. In this report, clinical features are described of this patient, along with the novel use of clonidine—a sympathetic blocking agent—in his treatment, published reports are reviewed on diencephalic seizures, and steps are recommended in the treatment of a patient who presents in this manner. The authors believe that diencephalic seizures can present with a spectrum of autonomic features, and treatment should be tailored with the appropriate pharmacologic blockade. © 1999 by Elsevier Science Inc. All rights reserved. Goh KYC, Conway EJ, DaRosso RC, Muszynski CA, Epstein FJ. Sympathetic storms in a child with a midbrain glioma: A variant of diencephalic seizures. Pediatr Neurol 1999;21:742-744.
From the *Pediatric Neurosurgery Unit; KK Women’s and Children’s Hospital; Singapore; and †Department of Pediatric Neurosurgery and Pediatric Critical Care Unit; Institute for Neurology and Neurosurgery; Beth Israel Medical Center (North Division); New York, New York.
742
PEDIATRIC NEUROLOGY
Vol. 21 No. 4
A 7-year-old male was referred for progressive headache associated with left hemiparesis and left facial palsy. Magnetic resonance imaging of the brain revealed the presence of a large tumor involving the midbrain and thalamus on the right (Fig 1). He underwent an image-guided (Viewing Wand, Elekta, Crawley, United Kingdom) craniotomy and partial surgical resection of the tumor (histologic finding of pilocytic astrocytoma). In the postoperative period, he had increased neurologic deficits, namely bilateral third nerve palsies, left facial nerve palsy, and spastic quadriparesis, which was worse on the left side. Within the first postoperative week, he began developing repeated episodes of tachycardia (150-180 bpm), hypertension (180/120 mm Hg), fever (38.4-39.5°C), sweating, muscle spasms, decorticate posturing, nystagmus, and teeth grinding. During these episodes, his oxygen saturation remained at 100%. An electroencephalogram (EEG) was performed that revealed diffuse slow-wave activity but no evidence of an epileptogenic focus. A computed tomography scan revealed no hydrocephalus or intraparenchymal hematoma. After a presumptive diagnosis of seizures, phenytoin was initiated and maintained at therapeutic levels with 100 mg twice daily. However, the episodes persisted, with frequencies of 4-6 times daily, and could only be controlled with benzodiazepines (Valium 1 mg every 6 hours or Ativan 1 mg intravenously as needed). The clinical impression was that these seizurelike episodes were periods of intense sympathetic hyperactivity, and clonidine was initiated at an initial dosage of 50 g every 12 hours. This dosage was increased eventually to 100 g every 8 hours after a good clinical response, and control of these episodes was achieved. The benzodiazepines were discontinued but phenytoin was maintained at 100 mg twice daily. The child continued to recover neurologically and was eventually sent for radiation therapy of his residual tumor. At 6 months follow-up, he had no tumor progression, phenytoin and clonidine were discontinued, and no further episodes occurred.
Communications should be addressed to: Dr. Goh; Pediatric Neurosurgery Unit; KK Women’s and Children’s Hospital; 100 Bukit Timah Road; Singapore 229 899. Received March 25, 1999; accepted June 2, 1999.
© 1999 by Elsevier Science Inc. All rights reserved. PII S0887-8994(99)00069-7 ● 0887-8994/99/$20.00
Figure 1. Axial T1-weighted magnetic resonance image (with contrast) (TR ⫽ 10,002, TE ⫽ 152/Ef) revealing the brightly enhancing lesion in the midbrain after partial surgical resection.
Discussion The term diencephalic seizures was first coined by Penfield [1] in 1929 to describe an atypical and uncommon form of what he thought was seizure activity in a patient with a tumor of the dorsal medial nucleus of the thalamus. In his patient, periodic episodes of headache, hypertension, vasodilatory changes in the skin, shivering, lacrimation, and pupillary change occurred, and eventually Cheyne-Stokes respiration and death. In 1934, 1945, and 1973, three patients with tumors involving the hypothalamus, thalamus, or hypothalamic-thalamic-third ventricle were reported as having such repeated autonomic episodes [2,5,6]. In 1987, Bullard [4] described two patients with severe diffuse head injury who developed episodes of increased temperature, respiratory rate, pulse, and blood pressure, diaphoresis, and extensor posturing. The computed tomography scans revealed no focal injury and EEGs again revealed only severe slowing. In 1988, Talman et al. [3] then reported two additional patients with similar autonomic episodes, this time with acute hydrocephalus. After shunting procedures were performed, the symptoms completely resolved without requiring medication. The most recently reported case was in 1998 from Boeve et al. [7], who described a 17-year-old female with a traumatic left temporal contusion and subarachnoid hemorrhage. The paroxysmal sympathetic storms in this patient were successfully treated with morphine sulphate. Typically, these episodes are characterized by changes in autonomic activity (i.e., body temperature, blood pressure, heart and respiratory rate, pupillary size, and sometimes hyperhidrosis, diaphoresis, and abnormal posturing, all of which occur in a paroxysmal fashion). Although sympathetic hyperactivity seems to predominate, episodes of hypothermia and bradycardia can occur as well, partic-
ularly when the etiology is related to congenital maldevelopment, such as in agenesis of the corpus callosum [8-12]. Other reported etiologies include tumors in the region of the thalamus and hypothalamus, head trauma, and acute hydrocephalus (Table 1). What is the underlying pathophysiology of these autonomic episodes? The original hypothesis was that these attacks were a form of epileptic activity, with the diencephalon implicated as the site at which damage led to seizurelike activity [1,2,5,6]. However, because no evidence for an epileptogenic focus has ever been demonstrated by EEG even during these episodes, and because most patients do not benefit from antiepileptic therapy, the term seizure is clearly a misnomer [4,8,11]. A review of all previously reported cases revealed evidence of either hydrocephalus or a lesion in the region of the brainstem or diencephalon. It has been suggested that ventricular dilatation, with subsequent rostral-caudal transtentorial herniation and brainstem compression, may lead to the intraventricular release of neuropeptides, inhibition of agents, such as endorphins, or the disruption of dopamine transmission from stretching of striatal dopaminergic fibers, thus resulting in disordered autonomic activity [3]. In one reported case, dilatation of the third ventricle caused medial hypothalamic dysfunction, which resolved after shunting [13]. Similarly, in the three patients with severe head trauma, it is possible that intermittent hydrocephalus or fluctuations in intracranial pressure may have contributed to the episodic signs. In the case of tumors that are present in the region of the diencephalon the pathophysiology is most likely an activation or a disinhibition of the central sympathoexcitatory regions, such as the paraventricular hypothalamic nucleus, lateral periaqueductal gray substance, or rostral ventrolateral medulla. Sympathetic excitation has been demon-
Goh et al: Sympathetic Diencephalic Seizures 743
Table 1.
Review of cases with automatic sympathetic seizures
Author
Patients (n)
Age (yr)
Penfield [1]
1
41
MacLean [5]
1
38
Engle and Aring [6] Solomon [2]
1 1
17 1
Bullard [4]
2
24; 24
Talman et al. [3]
2
26; 29
Boeve et al. [7]
1
17
Pathologic Findings Tumor: cholesteatoma left thalamus Tumor: astroblastoma hypothalamus Tumor: cyst left thalamus Tumor: astroblastoma hypothalamus and left thalamus Trauma: diffuse head injury (two patients) Acute hydrocephalus (two patients) Trauma: left temporal contusion
strated to occur in experimental neurogenic hypertension in which there are lesions in the hypothalamus or medulla [14]. Furthermore, activation of somatosympathetic spinal or medullary reflexes, which are triggered from muscle mechanoreceptors and chemoreceptors during episodes of hypertonia, likely have a contributory role as well [7]. It is important, therefore, to recognize the clinical features of these autonomic episodes and to treat them in an appropriate fashion. In this patient the sympathetic storms necessitated some form of blockade or suppression. Morphine sulphate and bromocriptine have been used successfully before. The mode of action is presumably from the peripheral suppressive effects of the opioids on somatosympathetic or vagal afferents and from modulation of dopaminergic pathways [4,7]. The choice of clonidine, which is an ␣-adrenergic agent used in the treatment of hypertension, was based on its action of stimulating the ␣-2-adrenoceptors in the brainstem, thus activating inhibitory neurons. The sympathetic outflow is reduced, leading to a drop in heart rate and reduced vasomotor tone. From this review, episodic autonomic dysfunction clearly occurs with variation in clinical features and secondary to various etiologies. The most important step in treating these patients is to first exclude a surgically treatable cause, such as hydrocephalus, that requires shunting, a tumor that requires resection, or a traumatic contusion or hematoma that should be evacuated. After excluding such causes the most appropriate pharmacologic intervention should be attempted to abolish these attacks.
744
PEDIATRIC NEUROLOGY
Vol. 21 No. 4
Medication
Outcome
Nil
Death
Nil
Death
Nil Phenytoin ⫹ primidone
Death Well controlled with both drugs
Morphine ⫹ bromocriptine Nil
Medication discontinued in one patient at 3 mo Resolution with ventriculoperitoneal shunting Medication discontinued at 3 mo
Morphine
References [1] Penfield W. Diencephalic autonomic epilepsy. Arch Neurol Psychiatry 1929;22:358-74. [2] Solomon GE. Diencephalic autonomic epilepsy caused by a neoplasm. J Pediatr 1973;83:277-80. [3] Talman WT, Florek G, Bullard DE. A hyperthermic syndrome in two subjects with acute hydrocephalus. Arch Neurol 1988;45:1037-40. [4] Bullard DE. Diencephalic seizures: Responsiveness to bromocriptine and morphine. Ann Neurol 1987;21:609-11. [5] McLean AJ. Autonomic epilepsy: Report of a case with observation at necropsy. Arch Neurol Psychiatry 1934;32:189. [6] Engle GL, Aring CD. Hypothalamic attacks with thalamic lesion. I. Physiologic and psychologic considerations. II. Anatomic considerations. Arch Neurol Psychiatry 1945;54:37-44. [7] Boeve BF, Wijdicks EFM, Benarroch EE, Schmidt KD. Paroxysmal sympathetic storms (diencephalic seizures) after severe diffuse axonal head injury. Mayo Clin Proc 1998;73:148-52. [8] Shapiro WR, Williams GH, Plum F. Spontaneous recurrent hypothermia accompanying agenesis of the corpus callosum. Brain 1969;92:423-36. [9] LeWitt PA, Newman RP, Greenberg HS, Rocher LL, Caine DB, Ehrenkranz JR. Episodic hyperhidrosis, hypothermia and agenesis of the corpus callosum. Neurology 1983;33:1122-9. [10] Carr-Locke D, Millac P. Diencephalic epilepsy in a patient with agenesis of the corpus callosum confirmed by computerised axial tomography. J Neurol Neurosurg Psychiatry 1977;40:808-14. [11] Summers GD, Young AC, Little RA, Stoner HB, Forbes WS, Jones RA. Spontaneous periodic hypothermia with lipoma of the corpus callosum. J Neurol Neurosurg Psychiatry 1981;44:1094-9. [12] Fox RH, Wilkins DC, Bell JA, et al. Spontaneous periodic hypothermia: Diencephalic epilepsy. BMJ 1973;2:693-5. [13] Darnell RB, Arbit E. Reversible diencephalic dysfunction: Episodic hyperhidrosis due to a trapped third ventricle. Neurology 1993;43:579-82. [14] Talman WT. Cardiovascular regulation and lesions of the central nervous system. Ann Neurol 1985;18:1-13.