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Show ORIGINAL CONTRIBUTION Migraine- like Visual Hallucinations as the Presenting Manifestations of Focal Seizures in Neurocysticercosis Sanjeev Jha, MD and Rajesh Kumar, MD Abstract: We report three patients with visual hallucinations as the initial manifestations of neurocysticercosis ( NCC) in whom migraine was the first diagnosis. The correct diagnosis was suspected when electroencephalograms were abnormal and was confirmed by characteristic brain imaging. The visual hallucinations ceased promptly after treatment with antiepileptic and anti- NCC medications. We caution that NCC may present with focal seizures manifesting as visual hallucinations with features of migraine. (/ Neuro- Ophthalmol 2007; 27: 300- 303) Positive visual phenomena such as flashes of light, geometric forms, and animate forms can be symptoms generated by dysfunction of the central nervous system in migraine or epilepsy ( 1). Elementary visual hallucinations, when combined with vomiting, headache, and blindness, are likely to be misdiagnosed as migraine ( 2,3). We report three patients who presented with migraine- like visual hallucinations as isolated manifestations of focal seizures in neurocysticercosis ( NCC), the most common helminthic infestation of the nervous system in developing countries, including India ( 4). CASE REPORTS Case 1 A 16- year- old girl complained of paroxysmal visual hallucinations for 14 months. They consisted of the sudden appearance of a fat man with a stick at frequencies varying from 2- 3 to 15- 20 per day. Each episode lasted for approximately 10- 20 seconds. Hallucinations were occasionally accompanied by flashing lights, moving snakes, and statues. They were almost always followed by mild headache, nausea, and vomiting, which persisted for 1 hour. The symptoms were exacerbated whenever she had insomnia. Department of Neurology, Sanjay Gandhi Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India. Address correspondence to Sanjeev Jha, MD, Additional Professor, Department of Neurology, Sanjay Gandhi PGIMS, Lucknow, India; E- mail: sjha@ sgpgi. ac. in Finding no ocular abnormalities, an ophthalmologist referred the patient to a family physician who diagnosed migraine and treated her for this. When there was no response to beta- blockers and triptans, psychiatrists were consulted who prescribed anxiolytics for a presumptive diagnosis of anxiety neurosis. When there was still no relief, a neurologic consultation was undertaken. An electroencephalogram ( EEG) revealed epileptiform discharges and brain MRI revealed a ring- like lesion in the occipital region with a prominent scolex ( Fig. 1). A presumptive diagnosis of NCC was made. Results of hematologic and biochemical investigations, including analysis of the cerebrospinal fluid, were normal. Perimetry revealed no visual field defects. She was treated with 15 mg/ kg/ day carbamazepine; 15 mg/ kg/ day albendazole, and 1 mg/ kg / day prednisone for 1 month. The hallucinations stopped within 4 days of starting treatment. She continues to be symptom- free and seizure- free after 8 months. Case 2 A 28- year- old man presented with a 1- year history of episodes of sudden diplopia, vertigo, and vomiting. The frequency of these episodes was 2- 6 per day. There was no tinnitus, hearing impairment, convulsion, or impairment of consciousness. Migraine was diagnosed, and he was treated with cinnarizine and betahistine to which he responded. He remained asymptomatic for 3 weeks, when he again developed diplopia. At the same time he reported seeing distorted multicolored zigzag lines lasting for 30- 45 seconds followed by mild headache, nausea, and occasional vomiting for 30- 60 minutes. The frequency of these episodes increased to 3- 4 per week as headache and vomiting also increased. Atypical migraine was again diagnosed, and he was given beta- blockers and flunarizine by a family physician, but there was no improvement. Complete ophthalmologic and neurologic examinations were normal, including formal visual fields. Results of hemogram, blood chemistry analysis, electrocardiography, and echocardiography were normal. An EEG revealed generalized paroxysmal epileptiform discharges. Brain MRI revealed multiple high signal ring- like lesions scattered bilaterally throughout both cerebral hemispheres ( Fig. 2). Lesions in the right caudate, right 300 J Neuro- Ophthalmol, Vol. 27, No. 4, 2007 Neurocysticercosis J Neuro- Ophthalmol, Vol. 27, No. 4, 2007 FIG. 1. Case 1. Axial FLAIR MRI reveals a ring- like lesion with scolex and perilesional edema in the right occipital area. thalamus, and bilateral occipital areas were large with perilesional edema. Some lesions were cystic and contained a scolex. The enzyme immunoassay for NCC in the cerebrospinal fluid ( CSF) was positive. CSF protein was elevated at 68 mg/ 100 mL, but glucose was normal at 58 mg/ 100 mL, and cell count was normal. He was treated with 15 mg/ kg/ day carbamazepine, 15 mg/ kg/ day albendazole, and 1 mg/ kg/ day prednisone for 30 days. The frequency of hallucinations decreased after 2 weeks, and there was no further vomiting. Prednisone was discontinued after diplopia subsided. He continues to be symptom- free at follow- up after 5 months. Case 3 A 41- year- old man presented with a 3- month history of seeing balls of fire jumping in front of his right visual field. These balls were multicolored, mainly bright red and yellow, and lasted for 15- 30 seconds. The frequency of these episodes was 2- 3 per week. Each episode was followed by an intense headache located mainly posteriorly. There were no associated convulsions or impairment of consciousness. There was no previous history of fever or exposure to drugs or toxins. Visual acuity and visual field testing were normal. There was early optic disc edema ( papilledema) in both FIG. 2. Case 2. Axial T2 MRI reveals multiple high signal ring- like lesions scattered throughout the cerebral hemispheres, including the right caudate, right thalamus, and bilateral occipital areas. eyes. Otherwise, the neuro- ophthalmologic and general physical examinations were normal. Results of the hemo-gram and blood chemistry analyses, including a thyroid profile, were normal. An EEG revealed paroxysmal generalized epileptiform discharges. A brain CT scan revealed multiple ring- enhancing granulomas and various stages of NCC in both cerebral hemispheres, including the occipital region ( Fig. 3). Acetazolamide at a dose of 375 mg/ day and 20 mg/ kg/ day sodium valproate were administered for 10 days. The patient had become symptom- free, and the papilledema had disappeared when he reported for a follow- up examination 3 months later. DISCUSSION Our three patients with NCC presented with visual hallucinations as manifestations of seizures of occipital lobe origin. Lesions of NCC were found on brain imaging in the occipital region. The diagnosis of NCC in these patients was confirmed on the basis of clinical, biochemical, 301 J Neuro- Ophthalmol, Vol. 27, No. 4, 2007 Jha and Kumar FIG. 3. Case 3. Axial post- contrast CT reveals multiple ring-enhancing lesions, including one in the left occipital area. radiologic, immunologic, and epidemiologic criteria ( 5) after excluding other etiologies mimicking NCC, such as tuberculous, fungal, or toxoplasma granulomas. Seizures are the most common presenting manifestations of parenchymal NCC, occurring in 50- 80% of patients ( 6,7). Potential mechanisms for the seizures are an inflammatory reaction to the parasite or mass effect ( 7,8). The seizures may consist solely of visual hallucinations, as occurred in our patients. The hallucinations may be elementary ( occipital lobe origin) or complex ( temporal lobe origin). The EEG is especially useful in showing the typical anterior sylvian abnormalities associated with seizures arising in the temporal lobe. The epileptogenic focus may be occipital with spread to the temporal lobe leading to clinical manifestations suggestive of temporal lobe origin. Independent contralateral temporal interictal and ictal discharges may also be found ( 9). Progress to temporal lobe structures is different and consistent with symptomatic occipital lobe epilepsy ( 10). The phenomenon of occipital lobe seizures spreading into anterior parts of the brain, primarily temporolimbic structures, has been well been described on the basis of depth electrode recordings ( 9,11- 14). Seizures manifesting strictly as visual hallucinations in many patients are initially misdiagnosed as migraine with aura, basilar migraine, or acephalgic migraine ( 15). Although the visual hallucinations of occipital seizures and those of the migraine aura have common features, they can be differentiated. The visual hallucinations of occipital seizures are mainly colored with circular patterns and often last for mere seconds ( 15). They often appear in the periphery of the temporal visual hemifield, becoming larger and frequently moving horizontally toward the midline ( 16). They are frequent, often occurring daily, and may be accompanied by eye and head deviation, illusions of eye movement, and repetitive eyelid closure or fluttering ( 13,14,17). Symptoms may progress to impairment of consciousness and generalized tonic- clonic activity ( 2). None of our patients reported blindness during the seizure episodes, but blindness may occur from the beginning ( 15). Associated headache may be ictal or postictal. Ictal headache is mild and rare. Postictal headache often associated with vomiting is frequent and lasts for 30 minutes- 1 hour. The visual auras of migraine start with predominantly flickering white linear and zigzag patterns in the center of the visual field and gradually expand over minutes toward the periphery of one hemifield, often leaving a temporary scotoma ( 18). They rarely occur as often as the hallucinations of occipital seizures ( 15). They may be associated with or progress to unilateral dysesthesias, hemiplegia, or dysphasia. Impairment of consciousness and convulsions are exceptional ( 2). Associated headache is typically unilateral, pulsating, and severe and is often associated with nausea and photophobia lasting for 4- 72 hours. Although migraine and epilepsy are distinct conditions with separate pathophysiologic mechanisms, they are found together in many patients and may even be causally related in some cases ( 19). Migraine attacks may follow partial complex seizures, particularly in adolescents and children. ( 20). Seizures may follow migraine attacks; intercalated seizures are those that occur between the migraine aura and the headache phase ( 21). Seizures induced by a classical migraine aura are almost always occipital in origin ( 22). Migralepsy- an old term used for " a seizure that may be a composite of symptoms encountered in epilepsy and migraine"- has recently been reintroduced ( 23,24). Basilar migraine may also be confused with seizures. This entity is usually seen in adolescent girls who subsequently develop common migraine ( 25). It is characterized by transient and fully reversible aura symptoms indicating focal dysfunction of the brain stem, the occipital lobes, or both, followed by headache ( 25- 27). Symptoms include visual loss or flashing lights, vertigo, dysarthria, bilateral paresthesias, and transient loss of consciousness. Aura symptoms gradually develop over 4 minutes and last less than 1 hour ( 15). The post- event headache may last for several hours ( 20). Attacks are usually infrequent and tend to stop with the passage of time ( 15). 302 © 2007 Lippincott Williams & Wilkins Neurocysticercosis J Neuro- Ophthalmol, Vol. 27, No. 4, 2007 Case 2 in this study initially presented with frequent episodes of sudden vertigo, vomiting, and diplopia, suggesting basilar migraine or vestibular neuronitis, a diagnosis supported by a response to vestibular sedatives. Reappearance of these features with prominent visual hallucinations was suggestive of basilar migraine, but the age, sex, and brief and frequent episodes of visual hallucinations did not support this diagnosis. The abnormal EEG, lesions in brain imaging, and response to antiepileptic medication supported the diagnosis of occipital seizures. 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