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8. De Kleermaeker FG, Bouwmans AE, Nicolai J, Klinkenberg S. Anterior opercular syndrome as a first presentation of herpes simplex encephalitis. J Child Neurol 2014;29:560‑3. 9. Adler AC, Kadimi S, Apaloo C, Marcu C. Herpes simplex encephalitis with two false‑negative cerebrospinal fluid PCR tests and review of negative PCR results in the clinical setting. Case Rep Neurol 2011;3:172‑8. 10. Sili U, Kaya A, Mert A; HSV Encephalitis Study Group. Herpes simplex virus encephalitis: Clinical manifestations, diagnosis and outcome in 106 adult patients. J Clin Virol 2014;60:112‑8.

intervention revealed a low‑grade glioma. Nocturnal seizure represents a significant diagnostic challenge for clinicians. Chest pain may occur after tonic‑clonic seizures.[1] Therefore, elevated serum CK is helpful for diagnosing generalized seizures.[2]

Hiroshi Nawashiro Department of Neurosurgery, Tokorozawa Central Hospital, Saitama, Japan E‑mail: [email protected]

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Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.141230

References 1.

Lee TH, Goldman L. Evaluation of the patient with acute chest pain. N Engl J Med 2000;342:1187‑95. 2. Libman MD, Potvin L, Coupal L, Grover SA. Seizure vs. syncope: Measuring serum creatine kinase in the emergency department. J Gen Intern Med 1991;6:408‑12. Access this article online Quick Response Code:

Received: 25‑05‑2014 Review completed: 15‑07‑2014 Accepted: 10‑08‑2014

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Elevated serum creatine kinase due to nocturnal seizure A previously healthy 25‑year‑old man complained of nightmares and chest pain in the morning. The result of his physical and neurological examination was normal except for a mild tenderness in the chest wall. Chest x‑ray and electrocardiographic screening were normal. Blood chemistry revealed increased creatine kinase (CK), which was further determined to be muscle‑specific CK (CK‑MM). Sleep electroencephalography showed spikes over the right hemisphere. Magnetic resonance imaging (MRI) of the brain revealed an abnormal hyperintensity area in the right mesial temporal lobe [Figure 1a, indicated with red square]. Proton MR spectroscopy at 3.0 T showed a decrease in N‑acetylaspartate (neuronal marker) [Figure 1b, arrow] and an increase in choline [Figure 1b, double arrows]. Surgical

a

b

Figure 1: (a) Magnetic resonance imaging of the brain revealed abnormal hyperintensity area in the right mesial temporal lobe. (b) Proton MR spectroscopy showed a decrease in N-acetylaspartate (neuronal marker) (arrow) and an increase in choline (double arrows)

Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4

DOI: 10.4103/0028-3886.141234

Received: 15‑06‑2014 Review completed: 06‑09‑2014 Accepted: 18‑06‑2014

Hypoventilation: An aid to the neurosurgeon Sir, We report the successful removal of a giant intracranial hydatid cyst in toto by Dowling’s hydrodissection technique with hypoventilation being used as an adjunct. An 8 year old girl with a large right parietooccipital  intra-parenchymal non‑enhancing cyst suggestive of hydatid cyst was planned for a right parieto‑occipital craniotomy and excision of the cyst [Figure 1]. In the operating room, standard monitoring with an electrocardiography (ECG), pulse oximetry, invasive blood pressure, and end tidal CO2  (etCO2) was commenced. After adequate preoxygenation, patient was intubated with 6.0  mm ID cuffed ETT. Anesthesia was maintained with isoflurane (MAC 0.8), oxygen, and air. Routine measures to reduce cerebral edema were undertaken- mannitol 1 gm/kg, dexamethasone 0.1 mg/kg, and an etCO2 of 28 mm Hg were maintained. After craniotomy, the dura was 435

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opened with careful separation of the arachnoid overlying the cyst. The lesion was visualized as a grayish white semi‑transparent cyst specked with the protoscolices lying just beneath the cyst wall. Using saline irrigation, hydrodissection of the cyst was performed. The etCO 2was gradually raised to 38 mm  Hg by hypoventilation and trendelenburg tilt was given to raise the intracranial pressure (ICP) to aid the delivery of the cyst. With gentle hydrodissection and the gradual rise in ICP, the cyst was delivered out of its cavity in to [Figures 2 and 3]. Normal ventilation was resumed, and the child was extubated fully awake and shifted to the neurosurgical intensive care unit. Carbon dioxide is a powerful cerebral vasodilator, thereby raising the ICP. [1] In most neurosurgical patients, it is desirable to reduce ICP and hence mild hyperventilation is used. This case is an exception

Figure 1: T2W axial MRI of the brain showing a large cystic lesion in the right posterior parietal and occipital lobes with significant mass effect

Figure 3: Empty cyst cavity after removal of the hydatid cyst

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wherein hypoventilation was initiated after exposure of the lesion. The resulting rise in arterial carbon dioxide tension causes increased cerebral blood flow, elevated ICP, thereby aiding delivery of the cyst in toto. Intracranial pressure can be raised by various methods such as intrathecal injection of air, intrathecal injection of saline, bilateral jugular venous compression, valsalva maneuver and by controlled hypercapnia.[2‑4] While use of Valsalva maneuvre to raise ICP and facilitate delivery of the hydatid cyst has been described, there is a risk of sudden and uncontrolled increase in ICP resulting in cyst rupture, which increases the chance of recurrence, cerebral vasospasm, and systemic inflammatory response syndrome.[5] A timely and gradual increase in ICP by hypoventilation as described in this case report is one of the adjunctive factors that aided in complete removal [Figure 4] of this intracranial hydatid cyst.

Figure 2: Intraoperative photograph of the translucent cyst after in toto excision

Figure 4: Post-operative plain computed tomography of the brain showing reduction in the mass effect and evidence of total excision of the cyst

Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4

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Karen Ruby Lionel, Georgene Singh, Rosen Roy Mathew, Ranjith K. Moorthy1, Vedantam Rajshekhar1 Departments of Anaesthesia and 1Neurological Sciences, Christian Medical College, Vellore, Tamil Nadu, India E‑mail: [email protected]

References 1.

Madden JA. The effect of carbon dioxide on cerebral arteries. Pharmacol Ther 1993;59:229‑50. 2. Hardy J. Transsphenoidal hypophysectomy. J Neurosurg 1971;34:582‑94. 3. Wilson CB, Dempsey LC. Transsphenoidal microsurgical removal of 250 pituitary adenomas. J Neurosurg 1978;48:13‑22. 4. Spaziante R, de Divitiis E. Forced subarachnoid air in transsphenoidal excision of pituitary tumors (pumping technique). J Neurosurg 1989;71:864‑7. 5. Salunke P, Patra DP, Mukherjee KK. Delayed cerebral vasospasm and systemic inflammatory response syndrome following intraoperative rupture of cerebral hydatid cyst. Acta Neurochir (Wien) 2014;156:613‑4. Access this article online Quick Response Code:

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room for emergency craniotomy. Through bi‑coronal skin incision, bilateral frontoparietal craniotomies were performed leaving a 3‑cm bone‑strip on the sinus sagittalis superior (SSS). The SSS was intact and the exact origin of the hemorrhage could not be identified. The hematoma was evacuated and dural hitch stitches were applied around the lateral edges of the craniotomies. The patient recovered well from the surgery and his triplegia completely improved. Postoperative MRI also revealed that the hematoma was completely evacuated [Figure 2]. The postoperative course was uneventful, and the patient was discharged in a stable condition. Vertex epidural hematomas  (VEH) account for only 8% of all EDH.[1,2] EDH located in other regions present themselves acutely. However, VEH does not follow the same pattern. The clinical symptoms of VEH may present several days after the trauma. Most cases with VEH present with non‑specific signs and symptoms, such as headache and vomiting.[1,2] A diagnostic dilemma arises from this non‑specific symptomatology. The leading symptom is severe headache, although vomiting, sensory complaints, nuchal rigidity, pupil edema, anisocoria, visual changes, seizures, and coma have all been

DOI: 10.4103/0028-3886.141239

Received: 16-06-2014 Review completed: 21-06-2014 Accepted: 10-08-2014

Vertex epidural hematoma and triplegia Sir, A 21‑year‑old man, a known patient of epilepsy, had a fall and struck his head during a generalized seizure on the day of admission. Neurological examination was unremarkable. An initial computed tomography (CT) of the head revealed neither hematoma nor skull fracture [Figure 1a]. After four hours of observation, the patient was discharged. Twenty‑four hours after the injury, the patient was re‑admitted to the emergency room with complaints of headache. During this admission, the patient was neurologically intact. Repeat head CT revealed no pathologies [Figure 1b]. Due to progressive headaches, the patient was hospitalized for further follow up. Fifty hours after the trauma, the patient became lethargic with progressive weakness of both legs and the right upper extremity. An emergent cranial magnetic resonance imaging (MRI) revealed a large epidural hematoma (EDH) of the vertex [Figure 1c and d]. Ten minutes after MRI, the patient suddenly became triplegic (both legs and the right upper extremity), and was rushed to the operating Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4

a

b

c

d

Figure 1: CT imaging at admission (a) and 24th hour post-trauma (b) were both normal. An MRI taken at the 50th hour post-trauma revealed a large vertex epidural hematoma (c, d)

Figure 2: Postoperative MRI revealed that the epidural hematoma was completely evacuated

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Hypoventilation: an aid to the neurosurgeon.

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