Year : 2007 | Volume
: 10 | Issue : 4 | Page : 240--246
Neurological complications of chickenpox
AS Girija, M Rafeeque, KP Abdurehman
Department of Neurology, Medical College, Calicut, Kerala - 673 008, India
A S Girija
Marathakam, Thiruthiyad, Calicut, Kerala - 673 004
Aim: To assess the neurological complications of chickenpox with prognosis. Background: The neurological complications occur in 0.03% of persons who get chickenpox. There is no universal vaccination against chicken pox in India. Most patients prefer alternate modalities of treatment. Hence these complications of chickenpox are likely to continue to occur. Study Design: A prospective study was conducted for 2 years (from March 2002) on the admitted cases with neurological complications after chickenpox (with rash or scar). Patients were investigated with CT/MRI, CSF study, EEG and nerve conduction studies and hematological workup. They were followed-up for 1 year and outcome assessed using modified Rankin scale. Results: The latency for the neurological complications was 4-32 days (mean: 16.32 days). There were 18 cases: 10 adults (64%) and 8 children (36%). Cerebellar ataxia (normal CT/MRI) was observed in 7 cases (32%) (mean age: 6.85 years). One patient (6 years) had acute right hemiparesis in the fifth week due to left capsular infarct. All these cases spontaneously recovered by 4 weeks. The age range of the adult patients was 13-47 years (mean: 27 years). The manifestations included cerebellar and pyramidal signs (n-4) with features of demyelination in MRI who recovered spontaneously or with methylprednisolone by 8 weeks. Patient with encephalitis recovered in 2 weeks with acyclovir. Guillain Barre syndrome of the demyelinating type (n-2) was treated with Intravenous immunoglobulin (IVIG) and they had a slow recovery by a modified Rankin scale (mRs) score of 3 and 2 at 6 months and 1 year, respectively. One case died after hemorrhage into the occipital infarct. There were two cases of asymmetrical neuropathy, one each of the seventh cranial and brachial neuritis. Conclusion: Spontaneous recovery occurs in post-chickenpox cerebellar ataxia. Rarely, serious complications can occur in adults. The demyelinating disorders, either of the central or peripheral nervous system, can be effectively managed using methylprednisolone or I/V IG.
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Girija A S, Rafeeque M, Abdurehman K P. Neurological complications of chickenpox.Ann Indian Acad Neurol 2007;10:240-246
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Girija A S, Rafeeque M, Abdurehman K P. Neurological complications of chickenpox. Ann Indian Acad Neurol [serial online] 2007 [cited 2020 Jul 14 ];10:240-246
Available from: http://www.annalsofian.org/text.asp?2007/10/4/240/37816
Chicken pox is mostly observed in pre-school and school-age children. In tropical climate, more cases are reported in adults (15 to 20% of affected cases).  The primary infection is characterized by generalized vesicular dermal exanthemas that are extremely contagious. After the primary infection, the virus may remain latent in the spinal and cranial ganglia neurons and then become reactive, thereby resulting in herpes zoster infection. Although the incidence is less in adults, serious complications can occur. The neurological complications of chickenpox is likely to continue as the disease affects the elderly, immunocompromized and because of the patients' preference for alternate modalities of treatment in spite of the availability of vaccine and specific drugs.
Neurological complications caused by chicken pox are estimated to be approximately 0.01-0.03%. Cerebellar ataxia and encephalitis are seen frequently, while transverse myelitis, aseptic meningitis, Guillain Barre syndrome, meningoencephalitis, ventriculitis, optic neuritis, post-hepatic neuralgia, herpes zoster ophthalmicus, delayed hemiparesis, peripheral motor neuropathy, cerebral angiitis, Reye's syndrome and facial paralysis are observed rarely. ,, Recently, larger numbers of patients do not acquire varicella until adolescence or young adulthood.  This shift in the age for varicella could have significant implications, as varicella tends to be a serious disease among adults. The mortality estimates for varicella in children (1 to 14 years) are 1.4/100,000 cases and in adults, the estimates are 31/100000 cases.  The most common causes of death in adults with chickenpox are pneumonitis and encephalitis. These reports are in the pre-vaccination era. As effective drugs are available now, this rate is likely to come down. This study was undertaken to document the neurological complications in varicella and the effectiveness of newer modalities of treatment
Materials and Methods
This study was performed for 2 years in the department from March 2002 to 2004. The cases of chickenpox with characteristic rash/scar and neurological complications and those admitted in the infectious wards of Medicine, Paediatrics and Neurology were included. The exclusion criteria were as follows: (1) delayed neurological deficit occurring without rash/scar; (2) preceding rash; and (3) cases of post herpetic complications. The patients were investigated by using CT or MRI of brain and spinal cord, CSF study, EEG and nerve conduction studies. I/V acyclovir was administered if the patients present within 1 week of the onset of symptoms. The cases of post-infectious demyelination showing changes of demyelination at multiple sites on MRI were treated with I/V methylprednisolone. The cases with Guillain Barre syndrome were treated with I/V IG. Oral acyclovir was given for the LMN complications; symptomatic treatment was provided to others. They were followed-up for1 year, and prognosis was assessed using modified Rankin scale (mRs).
There were a total of 18 cases: 8 children (Cerebellar ataxia
There were seven cases of pure cerebellar ataxia in children (mean age: 6.85 years). The mean time lag for the cerebellar symptoms after the rash was 10 days. The cerebellar manifestations included bilateral finger-nose incoordination in 6 slurred speech in 5 and gait ataxia in 7 cases. None of the cases had nystagmus. The CSF was normal in all the cases. Four of these patients had an MRI done, which was normal. CT was normal for the remaining three cases. Details of other 11 cases given in [Table 1],[Table 2].
A 43-year-old female was admitted on the fourth day of chickenpox with headache, vomiting, irrelevant talk and progressing to coma in two days. There was no history of convulsions and exposure to chickenpox. On examination, she had rash of chickenpox. She was in stupor and her glasgow coma scale (GCS) score was 9. There was no cranial nerve palsy, neck stiffness or signs of meningeal irritation. She was incontinent and was on a catheter and tube feeding. Investigations: Routine tests were normal. CT scan head was normal. EEG showed diffuse slowing in the delta range. CSF studies showed 94 mg of protein and 54 mg of sugar. No cells were observed. Treatment: Patient was given I/V Acyclovir 500 mg tds for 10 days. Patient had a gradual recovery over 2 weeks. When discharged on the fourteenth day, she was normal
Stroke in chickenpox
A 6-year-old male child was admitted with acute onset of weakness of right upper and lower limb on day 32 after the onset of chickenpox. There was no speech defect, No history of convulsion or delayed mile stones or family history of stroke. On examination, the boy was found to be conscious and alert. He had an IQ of 100. There was no defect in the cognitive function. He had right UMN facial palsy. Grade 2 motor power was present in the right upper and lower limbs. Reflexes were exaggerated on the right side. Right plantar was extensor. There were no signs of meningeal irritation.
Investigations: Hb 12 g; TC 8000; and DC P48 L 38E12 B2. Peripheral smear was normal. Sickling test was negative. ECG and ECHO were normal. CT head scan showed left gangliocapsular infarct. MR angiography was normal. Urine aminoacid screening was negative. Urine homocysteine was normal
Treatment: No specific drug treatment was given except physiotherapy.
Follow-up: By 1 month, the patient could walk independently. Motor power was grade 4
He had increased tone on Rt side. At the third month, he was completely normal with normal motor power. Right plantar was equivocal.
A 45-year-old man was admitted with a history of acute visual loss of Left eye on day 25 of chickenpox. There was no past history of visual complaints, diabetes or hypertension or IHD or dyslipidemia. He was a non-smoker and non-alcoholic. He had no perception of light in the left eye. By evening, he developed weakness of the right side of body. Then he was admitted to the hospital. Left fundus showed central retinal artery occlusion, which was confirmed by the ophthalmologist. He was alert; there was no dysphasia. There was right temporal field defect. He had grade 3 motor power in the right upper and lower limbs. The Carotid pulse was normal on both sides. Other systems were normal.
Investigations: TC 9500, DC P 56L 32 E 12, and ESR 60 mm/h. Postprandial blood sugar was 110 mg. Serum lipids were normal; ECG and ECHO were normal. CT head showed left MCA infarct. He was administered 150 mg aspirin. After 3 days, there was sudden deterioration. The patient became drowsy and GCS was 8; further, the weakness increased. Emergency CT scan showed hemorrhagic transformation of the infarct [Figure 2]. His blood studies revealed a platelet count of 15000. FDP was elevated. He was given 8 units of FFP. The patient's condition worsened, and he succumbed to his illness in 24 hrs.
Cerebellar ataxia with additional features and abnormal MRI
A 13-year-old female was admitted with unsteadiness, difficulty to walk and inappropriate laughter for 4 days. She had a rash and fever 16 days before. She had not taken drugs `nor was vaccinated for chickenpox. On examination, there was scar of chickenpox clustered over the trunk and face. The patient was alert and conscious. Higher cognitive functions were normal. She had emotional incontinence with spells of crying and laughter at times. Cranial nerves - there was bilateral UMN facial palsy. Motor system - grade 5 motor power in the upper limbs and grade 4 motor power in the lower limbs. All deep tendon reflex (DTR) were exaggerated. Both plantars were extensor. She also had cerebellar signs - finger-nose incoordination, dysdiadokokinesia, gait ataxia and slurred speech. There was no neck stiffness or other signs of meningeal irritation. Investigations: routine blood tests were normal. CSF showed the following: protein: 48 mg/dl and sugar:67 mg/dl. There were no cells. MRI brain and spinal cord showed multiple hypointense lesions in T1 that were hyper intense in T2. Nerve conduction studies with F waves, auditory and visual-evoked responses were normal. Treatment: This patient was given methyl prednisolone injection (1 g daily) for 3 days. Patient showed positive response by 5 days and could walk independently by 7 days. On follow-up after 1 month and 3 months, she was normal.
An 11-year-old male child, who was a sixth grade student, was admitted due to the paresis of both lower limbs with benumbed sensation occurring on day 18 of chickenpox, evolving in 3 days. He had not received any drug treatment for chickenpox. He could not turn in the bed nor sit up. He also had slurred speech and incoordination of upper limbs. On examination, the child was alert and conscious. His higher cognitive functions were normal. There was slurred speech. Finger nose in coordination of the upper limbs was present with grade 4 motor power. There was weakness of the trunk, and the patient could not turn in bed. Grade 2 symmetrical motor weakness was noticed in the lower limbs. There was blunting of all the modalities of sensations below D10. He was on an indwelling catheter for the retention of urine.
Investigations: Routine blood tests were normal. Lumbar CSF showed: protein - 65 mg/dl, sugar - 60 mg/dl and cells - 80/mm 3 (all lymphocytes). MRI of brain showed [Figure 1] hypointense lesions in T1, which were hyperintence in T2 in the brain stem and spinal cord showed similar lesions at the C2 level. Nerve conduction studies and evoked potential studies were normal. Patient was administered I/V methyl prednisolone 1 g daily for 3 days. He improved gradually over 2 weeks and after 1 month, he could walk with support; by 3 months, he was normal.
Cerebellar with additional features and normal MRI
A 37-year-old male was admitted on day 20 of rash with unsteadiness in walking and inability to carry out daily activities that progressed over 5 days. On examination, the patient was found to have scars of chicken pox. Neurological examination revealed normal higher functions and cranial nerves. Motor power was normal in the upper and lower limbs. All DTR were brisk and plantars were extensor. He had grade 1 horizontal nystagmus with a faster component towards the side of gaze on both sides. There was finger-nose incoordination and gait ataxia.
Investigations: Routine blood tests were normal. MRI of brain and spinal cord were normal. CSF showed the following: protein - 50 mg and sugar - 64 mg. No cells were observed.
Treatment: He was put on symptomatic treatment and physiotherapy. Patient had a full recovery in a week
A 24-year-old male, who was a manual laborer (educated up to fifth grade), was admitted with inappropriate laughter, irrelevant talk and behavior problems along with unsteadiness and weakness of limbs and incontinence of urine of one week duration, starting on day 16 after the onset of chickenpox. He had exposure to chickenpox at his workplace. On examination, his higher functions were found to be abnormal. He was not well-oriented in time and place. Comprehension defects were observed. His Mini Mental State Examinatin (MMSE) score was 21/30. His motor power was normal. All DTR were brisk; plantars were extensor. He had bilateral cerebellar signs with finger-nose incoordination and gait ataxia. He had urinary incontinence and lack of social inhibition. There were no signs of meningeal irritation.
Investigations: Routine blood tests were normal. EEG was normal. MRI of brain was normal. CSF study: protein - 54 mg and sugar - 68 mg; No cells were observed. The diagnosis was post-chickenpox Acute Disseminated Encephalomyelitis (ADEM). Treatment: Patient was subjected to symptomatic treatment
The higher functions of the patient improved in 1 week and MMSE improved to 24. He became continent at discharge. His long-tract signs reverted to normal in 1 month
A 45 year old male developed progressive weakness of both lowerlimbs, pain and paresthesia of feet on 25 th day of chickenpox. He was unable to sit and on standing with support he used to fall, which aggravated in darkness. He had no cranial symptoms. On examination, his higher functions and cranial nerves were normal. He had grade 4+ motor power in the upper limbs and grade 4− power in the lower limbs. Touch was impaired in the legs up to the ankle. Joint position was impaired till the inguinal region. Touch was impaired up to mid hand and joint position was impaired up to elbow. All DTR were absent. Plantars were flexor.
Investigation: Routine blood tests were normal. X-ray chest was normal; Serum electrolyte was normal. Urine: porphobilinogen negative. USG abdomen: Normal. CSF study: protein - 80 mg and sugar - 50 mg. Nerve conduction studies: Absence of sural, median and ulnar sensory potential. Motor conduction velocity showed distal latency prolongation with fall in the conduction velocity. F waves were absent in upper and lower limbs in the nerves tested. There was conduction block in left median nerves and right common peroneal nerves. Needle EMG of selected muscles showed a neurogenic pattern.
Patient was administered with I/V immunoglobulin 20 g daily for 5 days. He improved slowly with physiotherapy. He could sit up independently by 1 month. He had persistent sensory deficit on discharge. After 3 months, he had a mRs score of 3 and after 1 year it was 2.
A 14-year-old female (ninth grade student) was admitted with rapid onset weakness of upper and lower limbs in 3 days and deviation of angle of mouth to left and numbness of feet. On day 11 of chickenpox when she developed this. On examination, her higher functions were normal. There was lower motor neuron type facial palsy on right side. Grade 3 and Grade 2 motor weakness in the lower limbs were noticed. All DTR were absent. Joint position sense was impaired in the lower limbs up to the ankle. Other sensations were normal.
Investigation: Routine blood tests were normal. CSF studies: protein - 108 mg and sugar - 50 mg. No cells were observed. Nerve conduction studies showed fall in the conduction velocity in the lower limb nerves. F waves were absent. Distal latency was prolonged in the common peroneal nerve. Sensory conduction was prolonged in the sural nerve. Conduction was normal in the upper limbs Treatment: patient was put on I/V immunoglobulin 18 gm daily for 5 days along with physiotherapy.
She could walk with support by 1 month and independently by 3 months
A 31-year-old male was admitted with the deviation of angle of mouth to left, defective eye closure occurring on day 10 of chickenpox. He was a manual laborer and he had contacted the disease from his wife. On examination, he had right LMN facial palsy. There were no long tract signs. He underwent physiotherapy. He had a complete recovery by 4 weeks
A 20-year-old male was admitted with weakness in raising the arm on day 12 of chickenpox. There was no sensory complaint. He had nonspecific pain in the right shoulder prior to the onset of weakness. On examination, his higher functions and cranial nerves were normal. He had weakness of right serratus anterior with winging of the scapula [Figure 3]. Grade 3 weakness of right deltoid and biceps was also observed. Reflexes were normal. There was no sensory deficit.
Investigations: Routine blood tests - were normal. MRI cervical region was normal. Motor and sensory nerve conduction studies in the median and ulnar nerves were normal. Erb's point stimulation with pick up from serratus anterior in mid axillary line showed a latency of 4.2 ms on right side and 3.5 ms on left side.
Treatment: The patient underwent physiotherapy. He had complete recovery in a month.
Cerebellar ataxia is the most common neurological complication of chickenpox occurring in 1 in 4000 cases of children below 15 years. This was our experience with 7 children having isolated cerebellar ataxia. All of them had a benign course with spontaneous recovery. It accounts for more than one half of all the neurological complications of varicella-zoster virus (VZV) infection.  It is characterized by ataxia with nystagmus, headache, nausea, vomiting and nuchal rigidity. , The symptoms may begin as early as 11 days before and up to 21 days after the onset of the rash. , The examination of CSF in varicella-associated cerebellar ataxia reveals nonspecific findings with a cell count ranging from 0 to 68 cells/m. Lymphocytic pleocytosis and elevated protein may occur in 20-30% cases. The CSF glucose is normal and polymorphonuclear cells may be present in the early course of the disease. , In mild cases, no further evaluation is required.  This has been the observation in previous Indian reports as well.  The restriction of this manifestation to children may be related to the virus acting in the immature brain. No specific therapy, e.g., acyclovir, is indicated for this complication. ,, Neurological complications can antedate cutaneous eruptions, particularly in men. Detection of viral antigens by polymerase chain reaction can be helpful to diagnose such presentation. , CT and MRI are thus not mandatory in post-chickenpox pure cerebellar ataxia in children.
The incidence of chickenpox encephalitis is reported as 1/33000 cases.  Its occurrence is highest in adults (20 years) and infants.  Seizures occur in 29 to 52% cases. Focal neurological abnormality can include ataxia, hypertonia or hypotonia, hemiparesis, positive plantar responses, etc. The mortality of varicella encephalitis, excluding Reye's syndrome, varies from 5 to 10%.  Intranuclear inclusions and hemorrhagic necrosis, suggestive of varicella encephalitis, has been reported in immunocompromized patients and in neonates.  However, case 1 recovered in 2 weeks. This patient was presented on day 4, and he had the shortest latency in the series.
Varicella is an important risk factor for childhood ischemic stroke. Around 1/3 cases of stroke in children may be related to chickenpox.  Gangliocapsular infarcts as seen in our case (case 3) is commonly observed. , Hemiparesis, recurrent TIA, major arterial occlusion is significantly more in varicella-related cases of stroke. Most cases occur as a delayed complication of chickenpox as late as 1 year. Vasculitic changes, irregular stenosis and beading that involves multiple vessels have been described. The evidence of Varicella zoster virus within the vessel wall of diseased arteries is found on autopsy.  Viral migration from the trigeminal ganglion and nerve to the major cerebral arteries and further replication with thrombosis is the proposed mechanism. It usually takes a monophasic course with subsequent stenosis regression and occasional stenosis progression. 
Thrombocytopenia is a well known complication of chickenpox. It can occur in upto 1% cases.  It occurs early is, immune mediated and mild. The stroke could be attributed to infection as it had occurred within one month of chickenpox and no other etiological factors could be identified. The cause of death is raised intracranial pressure (ICP) due to hemorrhage in to the infracted brain. Thrombocytopenia is likely to be due to the septicemia that complicated chickenpox. Cerebral angiography could not be done. It is noteworthy that both cases of stroke had the longest latency after onset of rash.
The common clinical feature in the 4 cases (where ADEM can be suspected though MRI; it was positive in only 2 cases) is the cerebellar signs. Case 12 had quadriparesis with a sensory level at T10. The spinal MRI of this patient showed lesions in the cervical region that were hypointense in T1 and hyperintense in T2. In addition, Case 14 had pseudobulbar features. All these 4 patients recovered fully by 4 weeks with or without I/V methyl prednisolone. In the report by Murthy et al. ,  none had abnormality in MRI though ADEM was suspected. All the four cases occurred in the third week. Myelitis complicating varicella is extremely rare and accounts for only approximately 3% of neurological complications. None of the cases mentioned in this report had isolated transverse myelitis. The average latency for this complication has been reported as 8.25 days. CSF is abnormal with a pleocytosis not exceeding 160 white blood cells and the protein may be normal or moderately raised.  Neuromyelitis optica has been described following varicella.  The recovery of the cases of peripheral demyelination that resembled the Guillain Barre syndrome was relatively slow. They gained an mRs score of only 2 at 1 year even after I/V IG treatment. GBS accounts for 7% of the post-varicella neurological complications. The average interval between the appearance of rash and the onset of symptoms is 11.25 days with a range of 7-20 days. No specific diagnostic features distinguish the post-varicella GBS from cases due to other causes. ,
The asymmetrical neuropathies after chickenpox had a complete recovery [Table 2]. Facial palsy recovered in 3 weeks. Brachial neuritis recovered fully by 3 months. Facial paralysis as a complication of chicken pox is reported as a rare condition. It may even occur 5 days before the onset of the exanthem and during the 16-day period after chicken pox is diagnosed. , There is no reference for the occurrence of brachial neuritis in chickenpox.
The presence of varicella-zoster viral DNA, antibodies to varicella-zoster virus or both in the cerebrospinal fluid is a strong presumptive evidence of infection. Even the detection of antibodies in cerebrospinal fluid without the amplification of varicella-zoster viral DNA by PCR supports the diagnosis of infection of the nervous system.  The analysis of serum for antibodies is of no value, because the antibodies to varicella-zoster virus persist in serum in almost all adults.
The treatment benefit of acyclovir used routinely in immunologically competent children has not been proved. Acyclovir is of maximum benefit if it is used at the earliest.  As most patients had presented with complications after significant delay, it was not given except for case number 1 where it had only questionable benefit. I/V methyl prednisolone can be given to those who present with neurological deficits with a delay after onset (>7days) as these are likely to be cases of ADEM. Future studies should concentrate on the CSF serological studies and its correlation with treatment supported by investigations including MRI that will go a long way in the effective management of the neurological complications of chickenpox. Focus must be given for adults who are susceptible to occasional, although serious complications of chickenpox. Public education is required in this matter as most people seek alternate modalities of treatment. Use of chickenpox vaccination is the other alternative.
|1||Anne G. Varicella and Herpes zoster: Clinical disease and complications. Herpes 2006;13:2A -7A.|
|2||Caheid Y, Husein C. Severe neurological complications of chickenpox: Report of four cases. Eur J Gen Med 2005;2:177-9.|
|3||Gnann JW Jr. Varicella-Zoster virus: Atypical presentations and unusual complications. J Infect Dis 2002;186:S91-8.|
|4||LaGuardia JJ, Gilden DH. Varicella-zoster virus: A re-emerging infection. J Investig Dermatol Symp Proc 2001;6:183-7.|
|5||Choo PW, Donahue JG, Manson JE, Plott R. The epidemiology of varicella and its complications. J Infect Dis 1995;172:706-12.|
|6||Prblud SR. Varicell: Complications and cost. Paediatrics 1995;78 728-35.|
|7||Johnson R, Milbourn PE. Central nervous system manifestations of chickenpox. Can Med Assoc J 1970;102:831-4.|
|8||Straus SE, Ostrove JM, Inchauspe G, Felser JM, Freifeld A, Croen KD, et al. Varicella-zoster virus infections: Biology, natural history, treatment and prevention. Ann Intern Med 1988;108:221-37.|
|9||Peters AC, Versteeg J, Lindeman J, Bots GT. Varicella and acute cerebellar ataxia. Arch Neurol 1978;35:769-71.|
|10||Scheld WM, Whitley RJ, Durack DT. Infections of the central nervous system. Raven Press: New York, NY; 1991. p. 59.|
|11||Murthy JM. Acute disseminated encephalomyelitis. Neurol India 2002;50:238-43.|
|12||Goldston AS, Millichap JG, Miller RH. Cerebellar ataxia with preeruptive varicella. Am J Dis Child 1963;106:197-200.|
|13||Dangond F, Engle E, Yessayan L, Sawyer MH. Pre-eruptive varicella cerebellitis confirmed by PCR. Pediatr Neurol 1993;9:491-3.|
|14||Puchammar Stockl E, Popow-Kraupp T, Heinz FX, Mandi CW, Kanz C. Detection of zoster virus DNA by polymerase chain reaction in the cerebrospinal fluid of patients suffering from neurological complications associated with chickenpox or herpes zoster. J Clin Microbiol 1991;29:1513.|
|15||Preblud SR. Age specific risks of varicella complications. Paediatrics 1981;68:14-7.|
|16||McCormick WR, Rodnitzky RL, Schochet SS Jr, McKee AP. Varicella -zoster encephalomyelitis: A morphological and virological study. Arch Neurol 1969;21:559-70.|
|17||Ganesan V, Kirkham FJ. Mechanisms of ischemic stroke after chickenpox. Arch Dis Child 1997;76:522-5.|
|18||Askalan R, Suzanne L, Mayank S, Chan A, McGregor D, Andrew M, et al. Chickenpox and stroke in childhood. Stroke 2001;32:1257-62.|
|19||Silverstein S, Brunberg J. Post varicella basal ganglia infarction in children. Am J Neurol Radiol 1995;16:449-52.|
|20||Lanthier S, Armstrong D, Domi T, de Veber G. Post varicella arteriopathy of childhood: Natural history of vascular stenosis. Neurology 2005;64:660-3.|
|21||Murthy JM, Kishore TL. Neurological complications of chickenpox: A clinical, electrophysiological and MRI study. Neurol India 1996;44:195-201.|
|22||McCarthy JT, Amar J. Post varicella acute transverse myelitis: A case presentation and review of the literature. Paediatrics 1978;62:202-4.|
|23||Chusid MJ, Williamson SJ, Murphy JV, Ramey LS. Neuromyelitis optica following varicella infection. J Paediatr 1979;95:737-8.|
|24||McKendall RR, Klawans HL. Nervous system complications of varicella zoster virus in Handbook of clinical Neurology. In: Vinken PJ, Bruyn GW, editors. Amsterdam, North Holland; 1978. p. 161-83.|
|25||Miller HG, Stanton JB, Gibbons JL. Para infectious encephalomyelitis and related syndromes. Quarterly J Med 1956;298:427-505.|
|26||Deda G, Çaksen H, İağasıoğlu D, İnce E. A case of chickenpox associated with facial nerve palsy. Pediatr Dermatol 2002;19:95-6.|
|27||Gilden DH, Bennet JL, Kleinschmidt-DeMasters BK, Song DD, Yee AS, Steiner I. The value of cerebrospinal fluid antiviral antibody in the diagnosis of neurologic disease produced by varicella zoster virus. J Neurol Sci 1998;159:140-4.|
|28||Balfour HH Jr, Edelman CK, Anderson RS, Reed NV, Slivken RM, Marmor LH, Dix L, et al. Controlled trial of acyclovir for chickenpox evaluating time of initiation and duration of therapy and viral resistance. Pediatr Infect Dis J 2001;20:919-26.|