Letters to the Editor


A cryptic message in the brain Dear Sir, The science of medicine has developed by leaps and bounds over the years. However, the best intentions of physicians and the most well planned decisions may not do justice to the patients. We present a case where an atypical presentation and a resource limited investigation produced a misdiagnosis, an unnecessary intrusion into the brain and misery for all concerned. It was diagnosed as hemorrhage, post‑operative biopsy reported nothing and only reassessment pointed toward the direction of diagnosis. A 45‑year‑old diabetic woman came with left sided headache for 5 years which was severe in the early morning and was associated with projectile vomiting and photophobia. She observed progressive, painless loss of vision initially in her left eye and then the right eye. She was not even able to discriminate between colors. She had also developed double vision, which pronounced on looking towards the left side. To add to her troubles there was a progressive hearing loss of the left ear for the past 1 year.

Figure 1: Hypo density on the left cerebral convexity

Examination showed: Loss of abduction of the left eye, sensorineural deafness in the left ear and bilateral papilledema. Neck rigidity and Kerning’s sign were present. Investigations revealed: Normal blood work, hepatic and renal function tests. Chest X‑ray and echocardiography were also unremarkable. Computed tomography (CT) brain disclosed: A hypo density on the left cerebral convexity [Figure 1], with peripheral enhancement and a hyper density along the left tentorial leaf [Figure 2]. Patient was diagnosed as subdural hematoma and was subjected to surgery. However, biopsy report was: Dense fibro collagenous tissue. Figure 2: Hyper density along the left tentorial leaf

No specific infective or neoplastic pathology. In spite of surgery her symptoms did not subside and she came back 10 days later. CT brain [Figure 3] after the surgery was: Suggestive of pachymeningitis. Cerebrospinal fluid (CSF) analysis revealed elevated protein levels and Cryptococcal antigen positive. Patient was treated with amphotericin B 1  mg/kg/day (intravenously) plus flucytosine 100  mg/kg/day for 2  weeks, followed by fluconazole 6 mg/kg/day orally for 8 weeks. She recovered fully and has no complaints since then. Patient in question had presented with a clear cut history suggestive of a mass lesion compressing the brain from the left. The surgeon operated on her with the report from the CT scan as the condition was progressing and she needed immediate

Figure 3: Computed tomography brain after the surgery suggestive of pachymeningitis

Annals of Indian Academy of Neurology, October-December 2013, Vol 16, Issue 4


Letters to the Editor

intervention. When the biopsy report came in, it was clear that something had gone wrong. And when her symptoms recurred, it was obvious that the diagnosis was off the mark. The second brain imaging suggested a clue to the diagnosis. CSF analysis was the answer. With a mass lesion and papilledema there was a risk of death with the procedure. However, the progressive nature of the disease demanded a calculated risk. A guarded lumbar puncture was performed and the procedure was uneventful. In view of the patient’s diabetic[1] status, in addition to routine CSF analysis, a Cryptococcal antigen test was also ordered. This clinched the diagnosis and saved the patient. There have been several cases reported with Cryptococcal[2] and pneumococcal[3] meningitis masquerading as hemorrhage. The presenting features may be identical. Diabetes mellitus is a risk factor for both meningeal infections and cerebrovascular events. The one may be differentiated from the other by a guarded lumbar puncture for CSF analysis.[4] The case is quite instructive and humbling at the same time. It highlights the need for careful pre‑operative assessment and the importance of differential diagnosis in apparently straight forward presentations. It stresses the need for re‑evaluation and logical investigation even in post‑operative patients.

N. V. Sundarachary, A. Sridhar1 Departments of Neurology and 1General Medicine, Guntur Medical College, Guntur, Andhra Pradesh, India For correspondence: Dr. A. Sridhar, PG Hostel, Government General Hospital,

Guntur, Andhra Pradesh, India. E‑mail: [email protected]


Kushawaha A, Mobarakai N, Parikh N, Beylinson A. Cryptococcus neoformans meningitis in a diabetic patient – The perils of an overzealous immune response: A case report. Cases J 2009;2:209. 2. Hoque R, Gonzalez‑Toledo E, Jaffe SL. Cryptococcal meningitis presenting as pseudosubarachnoid hemorrhage. South Med J 2008;101:1255‑7. 3. Morgan LK. Pneumococcal meningitis masquerading as subarachnoid haemorrhage. Med J Aust 2003;179:559‑60;560. 4. Given CA 2 nd , Burdette JH, Elster AD, Williams DW 3 rd . Pseudo‑subarachnoid hemorrhage: A potential imaging pitfall associated with diffuse cerebral edema. AJNR Am J Neuroradiol 2003;24:254‑6. 1.

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Website: www.annalsofian.org

DOI: 10.4103/0972-2327.120444

The authors would like to thank the Department of Radiology, Guntur Medical College.

Magnetic resonance imaging and computed tomography scan findings in methanol poisoning Sir, I enjoyed reading the article titled “A rare presentation of methanol toxicity” that was published in your journal.[1] The authors mention that brain lesions typically described in methanol poisoning are in the form of hemorrhagic and non‑hemorrhagic necrosis of the basal ganglia and sub‑cortical white matter and to their knowledge, lesions in the parietal, temporal, or frontal areas of cerebrum and cerebellar hemispheres have rarely been reported in these patients to date. Therefore, after the presentation of the magnetic resonance imaging (MRI) findings in their patient’s brain, the authors state that their case is a rare presentation of infarct in bilateral parasagittal, parieto‑occipital and cerebellar regions of the brain. It should be noted that a previously published article, [2] however, gave information about 42 patients with acute methanol poisoning. Of them, 28  (66.6%) had a total of 55 pathological findings on their brain computed tomography (CT) scans, 5 (17.9%) and 7 (25%) of which were bilateral parasagittal hypodense white matter lesions in the occipital and frontal lobes, respectively. In addition, other

authors had not only previously reported the same lesions as that of the present Gupta’s case but also lesions in the frontal and temporal lobes in the brain CT and MRI of the methanol‑poisoned patients.[3‑13] This shows that the uni- or bilateral parasagittal, parietal, frontal, temporal, occipital, and cerebellar lesions seen on CT scan and MRI of the brain are documented and not rare complications of methanol poisoning although all these lesions may not concomitantly be present in a single case. If the authors had performed a simple search using PubMed, Google Scholar or SCOPUS, they could easily have retrieved the above‑mentioned studies. I suggest the authors to perform an accurate search for their review of the literature.

Hossein Sanaei‑Zadeh Emergency Room/Division of Medical Toxicology, Hazrat Ali‑Asghar (p) Hospital, Shiraz University of Medical Sciences, Shiraz, Iran

Annals of Indian Academy of Neurology, October-December 2013, Vol 16, Issue 4

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