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Show Journal of Clillical Neuro-ophtlu>/mo/ogy 8(2):81-83, 1988. Exercise-Induced Visual Hallucinations A Symptom of Occipital Lobe Tumors Simmons Lessell, M,D., and Jan Kylstra, M.D. t, 1988 Raven Press, Ltd., New York Two patients experienced unformed visual hallucinations in one hemifield but only with vigorous exercise. The hallucinations continued for years as an isolated symptom before an occipital tumor was demonstrated. Exercise-induced unformed visual hallucinations appear to be ictal phenomena and might be a specific symptom of occipital brain tumors. Key Words: Visual hallucinations-Occipital lobe tumors. From the Department of Ophthalmology, Harvard Medical School (S.L., ].K.), and the Neuro-ophthalmology Unit, Massachusetts Eye and Ear Infirmary (S.L.), Boston, Massachusetts. Address correspondence and reprint requests to Dr. S. Lessell at 243 Charles St., Boston, MA 02114, U.S.A. 81 Neurogenic visual hallucinations typically occur spontaneously, independently of the patient's activity. We present two apparently unique cases in which visual hallucinations that were precipitated by vigorous exercise proved to be the herald symptoms of occipital brain tumors. REPORT OF CASES Case One A healthy 56-year-old woman developed visual hallucinations while jogging. Her only significant medical history was of renal hypertension cured by reconstructive surgery 8 years earlier. She was not taking any medications. There was no personal or family history of migraine or any other neurological disorder. The episodes occurred only while jogging. Although she jogged daily, the hallucinations occurred only three or four times a year. They would not begin until she had been jogging for some time. Her hallucinations were stereotyped, limited to the right hemifield, and seemed to occur regardless of the ambient illumination. At the start of each episode, things to her right "looked a little on the doubled side." Soon she would see a horizontal "Vibrating line ... like a triangle of mountain peaks." Under the line she saw a "broad white vertical band." She would stop running when the hallucination started. The hallucination would persist for several minutes, disappear for about a minute, and then reappear for several minutes. She never checked if closing her eyes during an attack altered the hallucination. There were no associated symptoms, and following the hallucinations she felt entirely well and could resume jogging. At age 59 years she consulted her internist because she sometimes fleetingly felt "off balance." 82 S. LESSELL AND J. KYLsTRA Her general and neurological examinations were negative, but a computerized tomographic scan with contrast injection showed an extra-axial left occipital lesion that was interpreted as a meningioma. The patient had one of her typical visual hallucinations during the intravenous infusion of contrast medium while being scanned. It was the only hallucination that she experienced other than while jogging. Neuro-ophthalmological examination showed that her acuity was 20/15 both eyes and that her visual fields were full on the Goldmann perimeter to the I2e, Be, and I4e white stimuli. No abnormalities were evident on the remainder of the ophthalmological, neurological, or general physical examinations. An electroencephalogram showed no abnormalities. No attempt was made to "activate" the electroencephalogram by hyperventilation. Over the next few years, although her physical, radiological, and electroencephalographic findings remained unchanged, there was a change in her symptoms. The exercise-induced hallucinations were replaced by much more frequent hallucinations of a different character. These consisted of colored lights and circles moving in her right hemifield, predominantly in the upper quadrant. She reported that they lasted seconds to a minute and persisted with her eyes closed. There was now an aura of epigastric distress and a sensation of fear, without external provocation. Treatment with phenobarbital eliminated the aura and reduced the frequency of her hallucinatory attacks. Case Two A boy, healthy but for alcohol abuse, hallucinated a geometric pattern at irregular intervals during adolescence. This occurred only with heavy physical exertion, such as playing competitive hockey in high school. The hallucination was of four diamonds of various colors moving in a circle in the "corner on the right side." During each episode, which lasted 30 to 60 sec, he felt "spacey" but had no other symptoms and was able to continue his activities without ill effects. No images appeared on his left. He had no headaches and there was no family history of migraine or other neurological disorders. At age 17 years he had a generalized motor seizure during sleep. His general physical, neurological, and neuro-ophthalmological examinations gave normal results. Visual acuity and Goldmann visual fields were normal. An electroencephalo- ,.- !" ,\·,;thout hyperventilation), done shortly after the seizure and not repeated, showed slight generalized slowing but no focal abnormal~ties: His visual evoked responses to patterned stimuli were within normal limits. Computerized tomographic scanning demonstrated two enhancing nodules in the left occipitoparietal region surrounded by an area of low density that extended into the left occipital lobe. The mass appeared avascular on a carotid angiogram. Tissue obtained at open biopsy was interpreted histopathologically as a low-grade astrocytoma. The patient was started on Dilantin (ParkeDavis, Morris Plains, NJ) and never had another visual hallucination. However, one grand mal seizure occurred immediately after he discontinued the medication for a short time. Since surgery he has had a complete, macula-splitting right homonymous hemianopia, but over a 4 year period of follow-up there has been no change in his physical or radiographic findings. DISCUSSION There are many causes of visual hallucinations, but they can be classified pathogenetically into two groups. One group presumably results from direct stimulation or irritation of the cerebral cortex, and the other, indirectly, from reduced stimulation of the cerebral cortex (1). Cogan has designated these, respectively, as "ictal" and "release" hallucinations (2). Ictal hallucinations, unlike release hallucinations, are typically stereotyped from episode to episode and are more likely than the release hallucinations to be associated with other seizure manifestations. While ictal hallucinations are distinctly episodic, release hallucinations may be continuous or nearly so, intruding upon all of the patient's waking activities. Patients with release hallucinations usually have impaired visual acuity or field. Since the two patients described above had no impairment of visual function, no history of drug use at the time that their hallucinations began, and their hallucinations occurred at widely spaced intervals, it is likely that their hallucinations were from direct irritation or stimulation of the cerebral cortex: in other words, ictal hallucinations in the Cogan schema. The stereotyped nature of the visions from attack to attack and the association with other ictal phenomena also support this interpretation. The unformed nature of the visions is typical of the imagery that results from occipital stimulation and in cases of occipital seizures (3-6). What makes these cases unusual is that the visual hallucinations were precipitated by physical Dec/PITAL LOBE TUMORS 83 TABLE 1. Chemical and physiological alterations with exercise exertion. How might exercise precipitate ictal visual hallucinations? A survey of the vast literature on exertion cited in the Index Medicus (7-9) provides a myriad of possibilities (Table 1). Changes in pH, oxygen, carbon dioxide, and altered cerebral blood flow are some of the most obvious. Hyperventilation is a well-recognized means of eliciting pathological discharges during electroencephalography. The mechanism is uncertain, but cerebral blood flow is apt to be reduced as a consequence of the hypocarbia (10). In one electroencephalographic investigation of 476 brain tumor patients, hyperventilation precipitated pathological slowing in 36 patients (11). The slowing was recorded over the ipsilateral hemisphere Of, less commonly, bilaterally in supratentorial tumors. Whether the hyperpnea that is induced by exercise has electroencephalographic effects similar to those of hyperventilation at rest is unknown. Oxygen Carbon dioxide pH Potassium Vasodilation Lactate Proenkephalin Ammonia Opiates ~-Endorphin Vasopressin Aldosterone Prostacyclin From refs. 7-9. Temperature Blood pressure Pulse rate Hydration Glucose Tryptophan Melatonin Brain amines Growth hormone ACTH Renin Testosterone Cortisol Despite the many chemical and physiological alterations that accompany vigorous exertion, there is no evidence that patients with seizure disorders suffer adverse effects from exercise. Apart from injunctions concerning activities such as swimming alone that would place patients at special risk if they suffered a seizure, neurologists do not restrict exercise in epileptic patients. REFERENCES 1. Lessel S. Higher disorders of visual function: positive phenomena. In: Glaser JS, Smith JL, eds. Neuro-ophthalmology. Vol. 8. St. Louis: C.V. Mosby, 1975:27-44. 2. Cogan DG. Visual hallucinations as release phenomena. von Graefes Arch Klin Exp OphtalmoI1973;188:139-50. 3. Penfield W, Rasmussen T. The cerebral cortex of man: a clinical study of localization of function. New York: Hafner Publishing, 1968:136-47. 4. Teuber HL, Battersby WS, Bender MB. Visual field defects after penetrating missile wounds of the brain. Cambridge, MA: Harvard University Press, 1960:104. 5. Russell WR, Whitty CMW. Studies in traumatic epilepsy: III. Visual fits. I Neurol NeuroSllrg Psychiatr 1955;18:79-96. 6. Ludwig BI, Marsan CA. Clinical ictal patterns in epileptic patients with occipital electroencephalographic foci. Neurology 1975;25:463-71. 7. Cumulated Index Medicus, Vol. 25. Washington, D.C.: U.S. Government Printing Office, 1984:9312-23. 8. Cumulated Index Medicus, Vol. 26. Washington, D.C.: U.S. Government Printing Office, 1985:9459-71. 9. Cumulated Index Medicus, Vol. 27. Washington, D.C.: U.S. Government Printing Office, 1986:9957-69. 10. Goldensohn ES, Osborn MA. Activation procedures and other special methods of investigation in brain tumor. In: Hess R, ed. Handbook of electroencephalography and clinical neurophysiology, Vol. 14. Amsterdam: Elsevier, 1975:14-29. 11. Hess R. Significance of EEG signs for location of cerebral tumors. Electroenceplzalogr Clin NeurophysioI1961;19(suppl): 75. I Clin Nellra-aphthalmal, Vol. 8. No.2, 1988 |
