Letters to Editor
relief from seizures, phenytoin was substituted with
levetiracetam 1.5 g twice a day, and clobazam was
increased to 10 mg twice a day with clinical benefit.
Patient was hospitalized and investigated further.
Enhanced magnetic resonance imaging of brain was
normal and ictal electroencephalogram [Figure 1]
showed movement artefacts. Other investigations
revealed hypocalcemia (7.1 mg/dl), low serum vitamin
D3 (14 ng/ml) and mildly raised iPTH (80 pg/ ml).
She was given vitamin D injection 600,000 units
intramuscular, oral calcitriol sachet 60,000 IU per
week, and intravenous calcium gluconate followed
by oral calcium. The seizures gradually decreased
in frequency and amplitude and subsided with
the normalization of serum calcium (8.6 mg/dl).
Antiepileptic drugs were tapered. Patient is doing fine
with no seizures at one month of follow-up.
Hypocalcemia is known to cause increased neuronal
excitability and if a patient has epileptogenic
foci, hypocalcemia lowers the seizure threshold.
Acute hypocalcemia usually presents with perioral
numbness, tingling, laryngospasm, carpopedal spasm,
electrocardiographic changes, positive Chvostek and
Trousseau’s sign. Chronic hypocalcemia presents with
calcification of the basal ganglia and other parts of the
brain. There is ample literature on generalized tonic-
clonic, absence and focal seizures due to hypocalcemia
but epilepsia partialis continua due to hypocalcemia is a
very rare event. We could find only a single case report
of EPC due to hypocalcemia in world literature.[1]
In our patient there was a temporal relation between the
occurrence of EPC and nasal calcitonin spray. Seizures
ceased with the normalization of serum calcium. We feel
that hypocalcemia (due to vitamin D deficiency) might
have been precipitated by the nasal administration of
calcitonin. Calcitonin nasal spray-induced hypocalcemia
is very uncommon, especially in post-menopausal
Figure 1: EEG showing movement artifacts
Neurology India | Jul-Aug 2012 | Vol 60 | Issue 4
females.[2] However, there have been studies showing
that nasal calcitonin spray can transiently lead to
hypocalcemia.[3,4] To conclude, metabolic causes[5] should
be included in the differential diagnosis of causes
of EPC. Hypocalcemia should be considered as one
of the possible provocative agents for EPC in post-
menopausal females, more so when they don’t respond
to antiepileptic drugs.
Puneet Chhabra, Manish Modi1, Abhishek Garg1,
Sudesh Prabhakar1, Sanjay KR. Bhadada2
Departments of Internal Medicine, 1Neurology,
2
Endocrinology, Post Graduate Institute of Medical Education and
Research, Chandigarh - 160012, India
E-mail: modim72@yahoo.com
References
1. Belluzzo M, Monti F, Pizzolato G. A case of hypocalcemia-related
epilepsia partialis continua. Seizure 2011;20:720-2.
2. Thamsborg G, Storm TL, Brinch E, Sykulski R, Fogh-Andersen N,
Holmegaard SN, et al. The effect of different doses of nasal salmon
calcitonin on plasma cyclic AMP and serum ionized calcium. Calcif
Tissue Int 1990;46:5-8.
3. Buclin T, Randin JP, Jacquet AF, Azria M, Attinger M, Gomez F, et al.
The effect of rectal and nasal administration of salmon calcitonin in
normal subjects. Calcif Tissue Int 1987;41:252-8.
4. Thamsborg G. Effect of nasal salmon calcitonin on calcium and bone
metabolism. Dan Med Bull 1999;46:118-26.
5. Mao S, Liu Z, Ding M. Central pontine myelinolysis in a patient with
epilepsia partialis continua and hyperglycaemic hyperosmolar state.
Ann Clin Biochem 2011;48:79-82.
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PMID:
***
DOI:
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Received: 09-06-2012 Review completed: 10-06-2012 Accepted: 24-06-2012
Guillain-Barré syndrome as a
complication of typhoid fever
in a child
Sir,
Guillain-Barré syndrome (GBS) is a rare complication
of typhoid fever and only a few such cases have been
reported in the pediatric age group.[1-5]
A 2½-year-old child presented with fever of 20 days
433
 Letters to Editor

duration, not responding to medications (cefixime) to walk with support and the muscle power was 4/5
started after a blood culture growth of Salmonella typhi. in lower limbs. A final diagnosis of typhoid fever
The mother also noticed that the child had shown complicated with GBS was established.
a reluctance to walk since 4 days before admission.
On physical examination, child was febrile with a The most common neurological complication of typhoid
moderate degree of hepatosplenomegaly with pallor. fever is encephalopathy. [6,7] Other complications
Central nervous system examination was normal, include: Meningitis, catatonia, parkinsonism-like state,
except for reduced motor power (4/5) in both the benign intracranial hypertension, cranial nerve palsies,
lower limbs with hypoflexia. Investigations revealed: cerebellar ataxia, and GBS, which are rare.[1-5,8,9] The exact
Hemoglobin of 6.1g%, total leuckocyte count of pathogenesis of these complications is not known. It has
6500/cmm (polymorphs 56%, lymphocytes 46%, been postulated that toxemia, along with metabolic
monocytes 2%, and eosinophils 2%), and platelet count disturbances and non-specific cerebral changes such
of 4,06,000 per ul. Blood culture showed no growth, as edema and hemorrhage, may be responsible for
but a Widal test showed TO titre of 1:160, TH titre of encephalopathy.[10] Other possibilities that have been
1:160, AH titre of 1:80, and BH titer of 1:80. (normal suggested are hyperpyrexia, vasculitis, or autoimmune
value < 1:80). Ultrasonography of the abdomen revealed mechanisms.[4,11] The typhoid endotoxin may effect
hepatosplenomegaly. Based on the Widal test, a diagnosis any part of the central nervous system and may be
of typhoid fever was made, and the child was treated the possible mechanism behind the wide spectrum
with injectable ceftriaxone. On day-2 of admission, there of neurological complications of typhoid fever. [12]
A non-T-cell-dependent mechanism of generation
was worsening of power in both lower limbs (3/5) and
of IgM antibodies against some components of the
deep tendon reflexes were not elicitable on the next day.
bacterial capsule and their cross reactivity with myelin
CPK was normal. Suspecting a provisional diagnosis of
gangliosides has also been proposed for GBS in typhoid
GBS, cerebrospinal fluid (CSF) examination was done,
fever. [2] Unusual manifestations and neurological
which revealed 30 lymphocytes, protein of 234 mg/dl
complications may sometimes be confounding factors
and sugar 65 mg/dl. Electrodiagnostic studies revealed
in the diagnosis. Strict vigilance and a high index of
demyelinating type of motor and sensory neuropathy
suspicion are required to diagnose and treat these
[Table 1]. She was not given IVIg, because the general
complications timely, which may otherwise have
condition of the child started improving on supportive serious consequences.
therapy. By day-10 of admission, the child was able
Sumit Mehndiratta, Krishnan Rajeshwari1,
Table 1: NCV study of the patient Anand Prakash Dubey1
Motor NCS Department of Pediatrics, Lok Nayak Hospital,
Nerve/Sites Latency Amp Segments Distance Velocity 1
Department of Pediatrics, Maulana Azad Medical College,
ms 2-4 mv cm m/s New Delhi, India
L Median APB E-mail: drsmehndiratta@gmail.com
1. Wrist 7.80 2.0 1-0
2. Cubital fossa
L Ulnar –ADM
22.45 1.3 2-1 8.5 5.8
References
1. Wrist 7.45 2.7 1-0
2. Medial 25.05 1.6 2-1 8.5 4.8 1. Datta V, Sahare P, Chaturved P. Guillain-Barre syndrome as a
epicondyle complication of enteric fever. J Indian Med Assoc 2004;102:172-3.
R common 2. Aldrey JM, Fernández-Rial A, López-González FJ, Doval JC,
peroneal EDB de la Fuente-Fernández R. Guillain-Barré syndrome as first
1. Ankle 9.70 1.1 1-0 manifestation of typhoid fever. Clin Infect Dis 1999;28:1171-2.
3. Ozen H, Cemeroğlu P, Ecevit Z, Seçmeer G, Kanra G. Unusual neurologic
2. Fib head 25.55 0.8 2-1 11.5 7.3
complications of typhoid fever (aphasia, mononeuritis multiplex, and Guillain-
R Tibial (Knee) AH
Barré syndrome): A report of two cases. Turk J Pediatr 1993;35:141-4.
1. Ankle 6.05 1.0 1-0 4. May W, Senitiri I. Guillain-Barré syndrome associated with typhoid
2. Pop fossa 33.10 0.8 2-1 15 10.9 fever. A case study in the Fiji Islands. Pac Health Dialog 2010;16:85-8.
F Wave 5. Berger JR, Ayyar DR, Kaszovitz B. Guillain-Barré syndrome
Nerve Min F Lat Max F Lat Mean F Lat complicating typhoid fever. Ann Neurol 1986;20:649-50.
ms ms ms 6. Sharma A, Gathwala G. Clinical profile and outcome in enteric fever.
Indian Pediatr 1993;30:47-50.
L Median APB 32.25 35.85 33.88
7. Osuntokun BD, Bademosi O, Ogunremi K, Wright SG. Neuropsychiatric
L Ulnar ADM 35.50 36.45 35.92
manifestations of typhoid fever in 959 patients. Arch Neurol 1972;27:7- 13.
R Common Not
8. Ali G, Rashid S, Kamli MA, Shah PA, Allaqaband GQ. Spectrum of
Peroneal –EDB (1) recordable
neuropsychiatric complications in 791 cases of typhoid fever. Trop Med
R Tbial(Knee) - AH Not Int Health 1997;2:314-8.
recordable 9. Biswal N. Neurological manifestations of typhoid fever in children.
Right Sural: Not recordable J Trop Pediatr 1994;40:190.

434 Neurology India | Jul-Aug 2012 | Vol 60 | Issue 4

 Letters to Editor

10. Cohen JI, Bartlett JA, Corey GR. Extra-intestinal manifestations of there was no visualization of AVM in different positions.
salmonella infections. Medicine 1987;66:349-88.
11. Haque A. Neurological manifestations of entericfever. In: Chopra JS,
Sawhney IMS, editors. Neurologyin the Tropics. New Delhi: BI Churchill AVMs of the scalp consist of abnormally connecting
Livingstone; 1999. p. 506-12. arterial feeding vessels and draining veins, devoid of a
12. Ghosh JB, Senapati S. Palatal palsy in enteric fever. Indian Pediatr
2005;32:106-7.

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PMID:
***

DOI:
10.4103/0028-3886.100722

Received: 19-06-2012 Review completed: 20-06-2012 Accepted: 29-06-2012

Non filling of scalp Figure 1: Scalp AVM fed by greater occipital artery (arrows)

arteriovenous malformation:
Effect of position
Sir,
Scalp arteriovenous malformation (AVM) is an
uncommon condition and normally presents with
a boggy swelling, often pulsatile in nature. Though
there is risk of bleeding, treatment is often for cosmetic
reasons. The treatment options include surgical excision,
endovascular procedure and or combinations. We
present an interesting case of scalp AVM.

A 30-year-old female presented with progressive

boggy swelling in the right occipital region of five
years’ duration. Digital subtraction angiography Figure 2: Disappeared AVM with narrow feeding vessel (arrow) in supine
position
(DSA) revealed Type 1 scalp AVM[1] and was fed by
the greater occipital artery [Figure 1]. Patient was
taken for endovascular embolization 10 days after the
diagnostic DSA. During therapeutic embolization, no
AVM was seen [Figure 2]. Instead the feeding vessel
appeared to be very narrow in its lumen. For a while
it was thought that it might be a case of spontaneous
occlusion of artery. A re-look at the patient’s scalp
suggested that the feeding artery was getting kinked
by the head ring on which the patient’s head was lying.
The patient’s head was tilted to the opposite side by
10 to 15 degrees which resulted in refilling of the scalp
AVM. The feeding artery was selectively catheterized
[Figure 3] and embolization with N butyl-cynoacrylate
(NBCA) was completed. Check angiography showed no
residual AVM [Figure 4]. The therapeutic disappearance
of vascular lesion i.e. scalp AVM was only labeled when Figure 3: Selective catheterization and embolization of AVM

Neurology India | Jul-Aug 2012 | Vol 60 | Issue 4 435

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