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Year : 2004  |  Volume : 52  |  Issue : 3  |  Page : 378-379

Transitory alexia without agraphia: A disconnection syndrome due to neurocysticercosis

Department in Neurology, Institute of Medical Sciences, Banaras Hindu University, Varanasi - 221 005, India

Date of Acceptance06-Sep-2002

Correspondence Address:
Department in Neurology, Institute of Medical Sciences, Banaras Hindu University, Varanasi - 221 005, India

 » Abstract 

We describe a 65-year-old male who presented with acute onset inability to read, without any difficulty in writing. A clinical diagnosis of alexia without agraphia was made and the patient was subjected to routine investigations including contrast MRI. MRI showed a ring-enhancing lesion in left occipital area, suggestive of neurocysticercosis supported by quantitative enzyme-linked immunosorbant assay from purified cell fraction of taenia solium cysticerci (PCF­-ELISA). Patient was treated with albendazole and prednisolone for one week. The clinical manifestation as well as the radiological finding resolved after treatment.

How to cite this article:
Verma A, Singh N N, Misra S. Transitory alexia without agraphia: A disconnection syndrome due to neurocysticercosis. Neurol India 2004;52:378-9

How to cite this URL:
Verma A, Singh N N, Misra S. Transitory alexia without agraphia: A disconnection syndrome due to neurocysticercosis. Neurol India [serial online] 2004 [cited 2021 Jun 15];52:378-9. Available from:

 » Introduction Top

Alexia is defined as loss of reading ability in a previously literate person due to an acquired brain lesion. Alexia without agraphia (pure alexia) results from a lesion in the left occipital lobe and adjacent splenium (posterior corpus callosum) that disconnects visual input from language areas, first described by Dejerine.[1] The most common pathological process is usually an infarction in the territory of the posterior cerebral artery (PCA) due to occlusion by thrombi or emboli, although PCA compression during tentorial herniation and space occupying lesion may also cause this syndrome.[2],[3] We are reporting an unusual but interesting transitory cause of alexia without agraphia.

 » Case Report Top

A 65-year-old male, post-graduate, schoolteacher presented with acute onset difficulty in reading. He was able to name individual letters or numbers but could not read words or phrases. He retained the ability to speak, repeat speech, write and spell aloud. He was able to write a paragraph but was not able to read it back. There was no history suggestive of coronary artery disease, cerebro­vascular disease, trauma, blood transfusion, joint pain, rashes, photosensitivity, and seizure-like activity. The patient did not give any history of loss of consciousness, fever, headache, vomiting, dysphagia, dysarthria, gait ataxia or any weakness. There was no history suggestive of diabetes and hypertension.
The general physical examination and higher mental functions except for alexia were normal. At ophthalmic evaluation, right hemianopia was recorded. Visual acuity, including pupils, intraocular pressure and ocular fundi were normal. Patient had difficulty in reading and in naming colors but was able to match colors and shades. He was able to understand the nature and use of objects presented visually and recognize the faces. Both upper and lower limb bulk, power, reflex and plantar response were normal. Sensory and cerebellar examination were also normal.
Complete blood count, blood sugar, electrolyte, coagulation profile, collagen vascular profile, lipid profile, serum lactate and ELISA for HIV were normal. X-ray chest, carotid color doppler, ECG, echocardiogram were normal. EEG, CSF routine microscopy and PCR for HSV, and AFB were negative. Quantitative ELISA for immunodiagnosis of neurocysticercosis using cerebrospinal fluid showed a strongly positive result. CSF routine and microscopy revealed normal findings with normal lactate dehydrogenase (LDH) and R microglobulin. CT Scan (plain) was normal. Contrast magnetic resonance imaging (MRI) of brain revealed a ring-enhancing lesion 15 x 6 x 11 mm with perifocal edema in left occipital area on 2nd day of presentation [Figure - 1].
The patient was offered albendazole 15 mg/Kg body weight for 1 week along with steroid l-mg/Kg body weight for 1 week. There was a marked improvement and the patient was able to read. Follow-up MRI studies revealed complete resolution of the lesion after 8 weeks.

 » Discussion Top

In the classic syndrome of pure alexia without agraphia, patients can write but cannot read their own writing; speech, auditory comprehension, and repetition are normal. Naming deficit, especially for colors, may be present. Associated defi cits include a right hemianopia and frequently, a deficit of short-term memory.
The classic syndrome of pure alexia without agraphia is caused by lesion in left occipital cortex and posterior sector of the corpus callosum- (the splenium), thus interrupting the flow of visual input into the language network. There is usually a right hemianopia, but the core language network remains unaffected. Pure alexia may or may not be associated with color naming and visual object agnosia.
Transitory alexia without agraphia has been reported in a HIV positive patient suffering from toxoplasma encephalitis with ring lesion in left posterior white matter,[4] temporal lobe lesion due to herpes simplex encephalitis,[5] mitochondrial myopathy and lactic acidemia.[6]
In this communication, we describe a transitory non-vascular cause of alexia without agraphia, due to single ring-enhancing lesion in the left occipital area. Contrast MRI of the brain revealed a ring-enhancing lesion in the left occipital area disconnecting visual input from language area. The diagnosis of neurocysticercosis was based on the MRI finding, positive PCF-ELISA in CSF and the clinical manifestation as well as the resolution of radiological findings after treatment.
We concluded that our case report is an unusual non-epileptic manifestation of a very common endemic problem, neurocysticercosis. Reversible pure alexia has not been reported with neurocysticercosis. Recognizing this reversible cause will avoid unnecessary treatment and investigation of the patient. 

 » References Top

1.Dejerine J. Contribution a I'etude anatomo-pathologique et clinique des differentes varietes de cecites verbale. Memoires de la Societe Biologique 1892;4:61-90.  Back to cited text no. 1    
2.Caplan LR, Hedley-Whyte T. Cuing and memory dysfunction in alexia without agraphia. A case report. Brain 1974;97:251-62.  Back to cited text no. 2    
3.Cohen D, Salanga V, Hully W, Steinberg M, Hardy R. Alexia without agraphia. Neurol 1976;26:455-9.  Back to cited text no. 3    
4.Luscher C, Horber FF. Transitory alexia without agraphia in HIV positive patient suffering from toxoplasma encephalitis: A case report. Neurocase 2000;6:285.  Back to cited text no. 4    
5.Erdem S, Kansu T. Alexia without either agraphia or hemianopia in temporal lobe lesion due to herpes simplex encephalitis. J Neuro­ophthalmol 1995;15:102-4.  Back to cited text no. 5    
6.Skoglund RR. Reversible alexia, mitochondrial myopathy, and lactic acidemia. Neurol 1979;29:717-20.  Back to cited text no. 6    


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