- Email: [email protected]
Reversible congruous homonymous hemianopia as a symptom of shunt malfunction
Surg Neurol 1984;22:253-6
253
Reversible Congruous Homonymous Hemianopia as a Symptom of Shunt Malfunction Noriaki Kojima, M.D., Keiichi Kuwamura, M.D., Norihiko Tamaki, M.D., and Satoshi Matsumoto, M.D. Department of Neurosurgery, Kobe University School of Medicine, Kobe, Japan
Kojima N, Kuwamura K, Tamaki N, Matsumoto S. Reversible congruous homonymous hemianopia as a symptom of shunt malfunction. Surg Neurol 1984;22:253-6.
of this paper is to emphasize the early diagnosis of visual signs resulting from shunt malfunction.
Congruous left homonymous hemianopia occurred as a symptom of ventriculoperitoneal shunt malfunction. The low attenuation along the ventricular catheter in the right occipital area that was seen on a computed tomography scan disappeared after revision of the shunt, and corresponded with improvement of this peculiar visual field symptom. In view of anatomic considerations and clinical course, this homonymous field defect might be caused by peritubular cerebrospinal fluid edema in the right occipital area. In evaluating the patients having shunts, precise neuroophthalmologic examination should be performed for possible visual field defects.
Case R e p o r t
KEYWORDS: Hydrocephalus; Shunt malfunction; Congruous homonymous hemianopia; Cerebrospinal fluid edema; Computed tomography scar~
Signs and symptoms of shunt malfunction in hydrocephalic patients have already been reported on many occasions [1,6,10,12,21]. Not much attention, however, has been paid to possible visual field defects as symptoms in evaluating patients with malfunction of their shunts. On the other hand k is well known that a dilated third ventricle in hydrocephalus could cause some types of defects in the visual fields such as bitemporal [16,18,23], binasal [5], homonymous hemianopia [23]. To date there have been few reports describing precisely the cause of possible defects in the visual fields in patients with shunt malfunction [3,4]. To our best knowledge this is the first report dealing with a hydrocephalic patient who experienced two kinds of visual-field defect due to hydrocephalus and after shunt malfunction. The purpose
Address reprint request.~ to: Noriaki Kojima, M.D., Department of Neurosurgery, Kobe University School of Medicine, Chuoku Kusunokicho, 7-5-1, Kobe, 650, Japan.
© 1984 by Elsevier Science Publishing Co., Inc.
A 55-year-old woman was admitted to our neurosurgical service on June 25, 1982, because of worsening headache and rhinorrhea. She had been suffering from headaches and tinnitus for the last 25 years. Recently she had started to complain of loss of memory and disturbance of gait. Nine months before admission she had developed spontaneous nontraumatic rhinorrhea. The general physical examination was unremarkable on admission. Neuroophthalmologic examination revealed bilateral optic atrophy and binasal inferior quadrantanopia (Figure 1B), which she had never noticed. Her visual acuity was normal. Remaining cranial nerves were within normal limits. H er gait was unsteady, but her motor and sensory systems showed no abnormalities. Nasal discharge had a glucose content of 65 mg/dL. Plain x-ray films of the skull demonstrated increased digital markings, enlargement of the seUa turcica, and thinning of its floor. There was a bony defect in the anterior fossa around the cribriform plate on skull tomography. A computed tomography (CT) scan (Figure 1A) revealed marked symmetrical dilatation of lateral and third ventricles but the fourth ventricle was normal in size. Aqueductal stenosis was confirmed by pneumoencephalography and ventriculography. She underwent an operation and a ventriculoperitoneal (VP) shunt was installed. Soon after the operation, headache, tinnitus, and rhinorrhea disappeared, but her ventricular size did not change. Twenty days after the operation, she began to complain of a prominent visual field defect that she had never previously experienced. Precise neuroophthalmologic examination disclosed a congruous left homonymous hemianopia (Figure 2B), which was different from the type of field defect on admission (Figure 1B). We discovered that the flushing device of the shunt was hard to pump. A C T scan showed a low-density area 0090-3019/84/$3.00
254
Surg Neurol 1984;22:253-6
Kojima et al
I_
R
i!
i
B
Figure 1. (A) Computed tomography scan before VP shunt shows symmetrical dilatation of both lateral ventricles. (B) Binasal inferior quadrantanopia on the admission.
A along the ventricular catheter in the right occipital area (Figure 2A). On the 22nd day after the first operation, a surgical revision was performed after a diagnosis of shunt malfunction had been made. Operative findings disclosed that the abdominal portion of the catheter was obstructed with fibrous material. After this operation, her
subjective complaint of a defect in the visual fields disappeared completely, and examination of the visual fields 7 days after revision of the shunt disclosed again a binasal inferior quadrantanopia (Figure 3B). Disappearance of the low attenuation in the right occipital area was also shown on a CT scan (Figure 3A). Subsequent observation 1 year later revealed that her ventricular enlarge-
Figure 2. (A) Computed tomography scan 20 days after VP shunt when the patient began to complain of a left homonymous field defect. Low-density area along the ventricular catheter is seen in the right occipital region. (B) Chart of her visual fields on the same day as A demonstrates a congruous left homonymous hemianopia.
I_
A
B
R
Hemianopia from Shunt Malfunction
Surg Neurol 1984;22:253-6
I_
255
R
B
Figure 3. (A) Computed tomography scan 7 days after revision of the shunt. The low-density area around the shunt tract has disappeared. (B) Visual field examination taken on the same day as A discloses a binasal inferior quadrantanopia.
A
ment had been slightly reduced, but she still had a binasal inferior quadrantanopia, as on admission. Discussion Hydrocephalus may occasionally cause some kinds of visual field defects due to dilatation of the third ventricle [5,7,13-16,19,22]. Oppenheim [18] mentioned that an extreme distension of the third ventricle due to hydrocephalus might serve to press upon the optic chiasm and produce bitemporal hemianopsia. In 1912 Cushing and Walker [5] described neuroanatomic considerations of binasal hemianopia in hydrocephalic patients. They speculated that binasal hemianopia might be caused by the distended third ventricle pushing the optic nerves laterally against the carotid arteries. In our case, the patient showed bina~.~al inferior quadrantanopia on admission, which might be well explained by the theory of Cushing and Walker, or which might be caused by the compression of the upper surface of optic chiasm by the dilated third ventricle. This visual field defect did not improve in spite of installing a VP shunt. It is quite rare to see an improvement in visual field defects after treatment of hydrocephalus [5,15,16,19,22]. In many such patients--including our case--impairment of visual pathways might be quite irreversible due to longstanding mechanical compressive and distorting force with ventricu|omegaly. In 1941 Weinberger and Webster [23] stated that
homonymous hemianopia is produced by the stretching of optic tracts over the posterior communicating arteries by a dilated third ventricle. Homonymous hemianopia is classified as incongruous and congruous depending upon the site of lesion. Incongruous homonymous hemianopia indicates a contralateral lesion in the optic tract, while congruous homonymous hemianopia with macular sparing is characteristic of a contralateral lesion in the posterior part of the optic radiations [2,8]. Our patient developed a congruous left homonymous hemianopia when her VP shunt became blocked. Moreover this symptom was accompanied by a peritubular low-density area in the right occipital region on the CT scan, which was considered to be cerebrospinal fluid edema [4,17]. Both the congruous homonymous hemianopia and the low-density area on CT scan disappeared completely after revision of the shunt. Judging from these findings, it is appropriate to suppose that the lesion responsible for homonymous defect in her visual fields was the transient edema in the posterior part of right optic radiation as a result of malfunction of her shunt. This cerebrospinal fluid edema can be thought of as an initial stage toward postshunt porencephaly [9,11,20], which produces irreversible neurological sequelae. In order to avoid such unfavorable complication, it is necessary to make an early diagnosis of shunt malfunction. That is to say, while observing shunt patients with hydrocephalus in the outpatient clinic, especially when a shunt is inserted in the occipital region, one should per-
256
Surg N e u r o l 1984;22:253-6
form neuroophthalmologic examinations for possible defects in the visual fields as well as to check the shunt system and other clinical signs.
Kojima et al
12. 13.
References 1. Ames RH. Ventriculo-peritoneal shunts in the management of hydrocephalus. J Neurosurg 1967;27:525-9. 2. Block FC. Eye symptoms in brain tumors. 2nd ed. St Louis: Mosby, 1971:84-5. 3. Calogero JA, Alexander E. Unilateral amaurosis in a hydrocephalic child with an obstructed shunt. J Neurosurg 1971 ;34:23640. 4. Chiba Y, Takagi H, Nakajima F, Fujii S, Kitahara T, Yagishita S, Itoh Y. Cerebrospinal fluid edema: a rare complication of shunt operations for hydrocephalus. J Neurosurg 1982;57:697-700. 5. Cushing H, Walker CB. Distortions of visual field in cases of brain tumors, binasal hemianopsia. Arch Ophthalmol 1912 ;41:55998. 6. Davidson RI, Lingley JF. Intraperitoneal pseudocyst: treatment by aspiration. Surg Neurol 1975;4:33-6. 7. Duke-Elder. System of ophthalmology, neuro-ophthalmology. Vol 12. London: Kimpton, 1971:389-91. 8. Duke-Elder. System of ophthalmology, neuro-ophthalmology. Vol 12. London: Kimpton, 1971:425-6. 9. Epstein F, Naidich T, Kircheff I, Chase N, Lin J, Ransohoff J. Role of computerized axial tomography in diagnosis, treatment, and follow-up of hydrocephalus. Preliminary communication. Child's Brain 1977;3:91-100. 10. Fischer EG, Shillito J. Large abdominal cysts: a complication of peritoneal shunts. J Neurosurg 1969;31:441-4. 11. Fujita K, Hirayama H, Kusunoki T, Tamaki N, Matsumoto S.
14.
15. 16. 17.
18.
19.
20.
21. 22.
23.
Postshunt porencephaly as a complication of shunt in hydrocephalus. Monogr Neural Sci. Vol 8. Basel: Karger, 1982:92-5. Grifford RRM, Plaut CMR. Abdominal catheter retraction in a ventriculoperitoneal shunt. Clin Pediatr 1974;13:84-5. Harrison MJD, Robert CM, Uttley D. Benign aqueductal stenosis in adults. J Neurol Neurosurg Psychiatry 1974;37:1322-8. Humphrey PRD, Moseley IF, Russel RWR. Visual field defects in obstructive hydrocephalus. J Neurol Neurosurg Psychiatry 1982;45:591-7. Lassman LP, Cullen JF, Howat JML. Stenosis of the aqueduct of Sylvius. Am J Ophthalmol 1960;49:261-6. Little JR, Houser OW, MacCarty CS. Clinical manifestations of aqueductal stenosis in adults. J Neurosurg 1975;43:546-52. Marmarou A, Takagi H, Shulman K. Biomechanics of brain edema and effects on local cerebral blood flow. In: Cerv6s-Navarro J, Ferszt R, eds. Brain edema. Pathology, diagnosis, and therapy. Advances in neurology. Vo128. New York: Raven Press, 1980:34558. Oppenheim H. Text book of nervous disease for physicians and students. (Translated by A. Bruce.) Vol 2. Edinburgh: O Schulze & Co, 1911:921. Osher RH, Corbett JJ, Schatz NJ, Savino PJ, Orr LS. Neuroophthalmological complications of enlargement of the third ventricle. Br J Ophthalmol 1978;62:536-42. Palmieri A, Pasquini U, Menichelli F, Salvolini U. Cerebral damage following ventricular shunt for infantile hydrocephalus evaluated by computed tomography. Neuroradiology 1981 ;21 :33-5. Sayers MP. Shunt complications. Clin Neurosurg 1976;23:393400. Sinclair AHH, Dott NM. Hydrocephalus simulating tumor in the production of chiasmal and other parahypophysial lesions. Trans Ophthal Soc UK 1931;51:232-46. Weinberger LM, Webster JE. Visual field defects associated with cerebellar tumors. Arch Ophthalmol 1941;25:128-38.
253
Reversible Congruous Homonymous Hemianopia as a Symptom of Shunt Malfunction Noriaki Kojima, M.D., Keiichi Kuwamura, M.D., Norihiko Tamaki, M.D., and Satoshi Matsumoto, M.D. Department of Neurosurgery, Kobe University School of Medicine, Kobe, Japan
Kojima N, Kuwamura K, Tamaki N, Matsumoto S. Reversible congruous homonymous hemianopia as a symptom of shunt malfunction. Surg Neurol 1984;22:253-6.
of this paper is to emphasize the early diagnosis of visual signs resulting from shunt malfunction.
Congruous left homonymous hemianopia occurred as a symptom of ventriculoperitoneal shunt malfunction. The low attenuation along the ventricular catheter in the right occipital area that was seen on a computed tomography scan disappeared after revision of the shunt, and corresponded with improvement of this peculiar visual field symptom. In view of anatomic considerations and clinical course, this homonymous field defect might be caused by peritubular cerebrospinal fluid edema in the right occipital area. In evaluating the patients having shunts, precise neuroophthalmologic examination should be performed for possible visual field defects.
Case R e p o r t
KEYWORDS: Hydrocephalus; Shunt malfunction; Congruous homonymous hemianopia; Cerebrospinal fluid edema; Computed tomography scar~
Signs and symptoms of shunt malfunction in hydrocephalic patients have already been reported on many occasions [1,6,10,12,21]. Not much attention, however, has been paid to possible visual field defects as symptoms in evaluating patients with malfunction of their shunts. On the other hand k is well known that a dilated third ventricle in hydrocephalus could cause some types of defects in the visual fields such as bitemporal [16,18,23], binasal [5], homonymous hemianopia [23]. To date there have been few reports describing precisely the cause of possible defects in the visual fields in patients with shunt malfunction [3,4]. To our best knowledge this is the first report dealing with a hydrocephalic patient who experienced two kinds of visual-field defect due to hydrocephalus and after shunt malfunction. The purpose
Address reprint request.~ to: Noriaki Kojima, M.D., Department of Neurosurgery, Kobe University School of Medicine, Chuoku Kusunokicho, 7-5-1, Kobe, 650, Japan.
© 1984 by Elsevier Science Publishing Co., Inc.
A 55-year-old woman was admitted to our neurosurgical service on June 25, 1982, because of worsening headache and rhinorrhea. She had been suffering from headaches and tinnitus for the last 25 years. Recently she had started to complain of loss of memory and disturbance of gait. Nine months before admission she had developed spontaneous nontraumatic rhinorrhea. The general physical examination was unremarkable on admission. Neuroophthalmologic examination revealed bilateral optic atrophy and binasal inferior quadrantanopia (Figure 1B), which she had never noticed. Her visual acuity was normal. Remaining cranial nerves were within normal limits. H er gait was unsteady, but her motor and sensory systems showed no abnormalities. Nasal discharge had a glucose content of 65 mg/dL. Plain x-ray films of the skull demonstrated increased digital markings, enlargement of the seUa turcica, and thinning of its floor. There was a bony defect in the anterior fossa around the cribriform plate on skull tomography. A computed tomography (CT) scan (Figure 1A) revealed marked symmetrical dilatation of lateral and third ventricles but the fourth ventricle was normal in size. Aqueductal stenosis was confirmed by pneumoencephalography and ventriculography. She underwent an operation and a ventriculoperitoneal (VP) shunt was installed. Soon after the operation, headache, tinnitus, and rhinorrhea disappeared, but her ventricular size did not change. Twenty days after the operation, she began to complain of a prominent visual field defect that she had never previously experienced. Precise neuroophthalmologic examination disclosed a congruous left homonymous hemianopia (Figure 2B), which was different from the type of field defect on admission (Figure 1B). We discovered that the flushing device of the shunt was hard to pump. A C T scan showed a low-density area 0090-3019/84/$3.00
254
Surg Neurol 1984;22:253-6
Kojima et al
I_
R
i!
i
B
Figure 1. (A) Computed tomography scan before VP shunt shows symmetrical dilatation of both lateral ventricles. (B) Binasal inferior quadrantanopia on the admission.
A along the ventricular catheter in the right occipital area (Figure 2A). On the 22nd day after the first operation, a surgical revision was performed after a diagnosis of shunt malfunction had been made. Operative findings disclosed that the abdominal portion of the catheter was obstructed with fibrous material. After this operation, her
subjective complaint of a defect in the visual fields disappeared completely, and examination of the visual fields 7 days after revision of the shunt disclosed again a binasal inferior quadrantanopia (Figure 3B). Disappearance of the low attenuation in the right occipital area was also shown on a CT scan (Figure 3A). Subsequent observation 1 year later revealed that her ventricular enlarge-
Figure 2. (A) Computed tomography scan 20 days after VP shunt when the patient began to complain of a left homonymous field defect. Low-density area along the ventricular catheter is seen in the right occipital region. (B) Chart of her visual fields on the same day as A demonstrates a congruous left homonymous hemianopia.
I_
A
B
R
Hemianopia from Shunt Malfunction
Surg Neurol 1984;22:253-6
I_
255
R
B
Figure 3. (A) Computed tomography scan 7 days after revision of the shunt. The low-density area around the shunt tract has disappeared. (B) Visual field examination taken on the same day as A discloses a binasal inferior quadrantanopia.
A
ment had been slightly reduced, but she still had a binasal inferior quadrantanopia, as on admission. Discussion Hydrocephalus may occasionally cause some kinds of visual field defects due to dilatation of the third ventricle [5,7,13-16,19,22]. Oppenheim [18] mentioned that an extreme distension of the third ventricle due to hydrocephalus might serve to press upon the optic chiasm and produce bitemporal hemianopsia. In 1912 Cushing and Walker [5] described neuroanatomic considerations of binasal hemianopia in hydrocephalic patients. They speculated that binasal hemianopia might be caused by the distended third ventricle pushing the optic nerves laterally against the carotid arteries. In our case, the patient showed bina~.~al inferior quadrantanopia on admission, which might be well explained by the theory of Cushing and Walker, or which might be caused by the compression of the upper surface of optic chiasm by the dilated third ventricle. This visual field defect did not improve in spite of installing a VP shunt. It is quite rare to see an improvement in visual field defects after treatment of hydrocephalus [5,15,16,19,22]. In many such patients--including our case--impairment of visual pathways might be quite irreversible due to longstanding mechanical compressive and distorting force with ventricu|omegaly. In 1941 Weinberger and Webster [23] stated that
homonymous hemianopia is produced by the stretching of optic tracts over the posterior communicating arteries by a dilated third ventricle. Homonymous hemianopia is classified as incongruous and congruous depending upon the site of lesion. Incongruous homonymous hemianopia indicates a contralateral lesion in the optic tract, while congruous homonymous hemianopia with macular sparing is characteristic of a contralateral lesion in the posterior part of the optic radiations [2,8]. Our patient developed a congruous left homonymous hemianopia when her VP shunt became blocked. Moreover this symptom was accompanied by a peritubular low-density area in the right occipital region on the CT scan, which was considered to be cerebrospinal fluid edema [4,17]. Both the congruous homonymous hemianopia and the low-density area on CT scan disappeared completely after revision of the shunt. Judging from these findings, it is appropriate to suppose that the lesion responsible for homonymous defect in her visual fields was the transient edema in the posterior part of right optic radiation as a result of malfunction of her shunt. This cerebrospinal fluid edema can be thought of as an initial stage toward postshunt porencephaly [9,11,20], which produces irreversible neurological sequelae. In order to avoid such unfavorable complication, it is necessary to make an early diagnosis of shunt malfunction. That is to say, while observing shunt patients with hydrocephalus in the outpatient clinic, especially when a shunt is inserted in the occipital region, one should per-
256
Surg N e u r o l 1984;22:253-6
form neuroophthalmologic examinations for possible defects in the visual fields as well as to check the shunt system and other clinical signs.
Kojima et al
12. 13.
References 1. Ames RH. Ventriculo-peritoneal shunts in the management of hydrocephalus. J Neurosurg 1967;27:525-9. 2. Block FC. Eye symptoms in brain tumors. 2nd ed. St Louis: Mosby, 1971:84-5. 3. Calogero JA, Alexander E. Unilateral amaurosis in a hydrocephalic child with an obstructed shunt. J Neurosurg 1971 ;34:23640. 4. Chiba Y, Takagi H, Nakajima F, Fujii S, Kitahara T, Yagishita S, Itoh Y. Cerebrospinal fluid edema: a rare complication of shunt operations for hydrocephalus. J Neurosurg 1982;57:697-700. 5. Cushing H, Walker CB. Distortions of visual field in cases of brain tumors, binasal hemianopsia. Arch Ophthalmol 1912 ;41:55998. 6. Davidson RI, Lingley JF. Intraperitoneal pseudocyst: treatment by aspiration. Surg Neurol 1975;4:33-6. 7. Duke-Elder. System of ophthalmology, neuro-ophthalmology. Vol 12. London: Kimpton, 1971:389-91. 8. Duke-Elder. System of ophthalmology, neuro-ophthalmology. Vol 12. London: Kimpton, 1971:425-6. 9. Epstein F, Naidich T, Kircheff I, Chase N, Lin J, Ransohoff J. Role of computerized axial tomography in diagnosis, treatment, and follow-up of hydrocephalus. Preliminary communication. Child's Brain 1977;3:91-100. 10. Fischer EG, Shillito J. Large abdominal cysts: a complication of peritoneal shunts. J Neurosurg 1969;31:441-4. 11. Fujita K, Hirayama H, Kusunoki T, Tamaki N, Matsumoto S.
14.
15. 16. 17.
18.
19.
20.
21. 22.
23.
Postshunt porencephaly as a complication of shunt in hydrocephalus. Monogr Neural Sci. Vol 8. Basel: Karger, 1982:92-5. Grifford RRM, Plaut CMR. Abdominal catheter retraction in a ventriculoperitoneal shunt. Clin Pediatr 1974;13:84-5. Harrison MJD, Robert CM, Uttley D. Benign aqueductal stenosis in adults. J Neurol Neurosurg Psychiatry 1974;37:1322-8. Humphrey PRD, Moseley IF, Russel RWR. Visual field defects in obstructive hydrocephalus. J Neurol Neurosurg Psychiatry 1982;45:591-7. Lassman LP, Cullen JF, Howat JML. Stenosis of the aqueduct of Sylvius. Am J Ophthalmol 1960;49:261-6. Little JR, Houser OW, MacCarty CS. Clinical manifestations of aqueductal stenosis in adults. J Neurosurg 1975;43:546-52. Marmarou A, Takagi H, Shulman K. Biomechanics of brain edema and effects on local cerebral blood flow. In: Cerv6s-Navarro J, Ferszt R, eds. Brain edema. Pathology, diagnosis, and therapy. Advances in neurology. Vo128. New York: Raven Press, 1980:34558. Oppenheim H. Text book of nervous disease for physicians and students. (Translated by A. Bruce.) Vol 2. Edinburgh: O Schulze & Co, 1911:921. Osher RH, Corbett JJ, Schatz NJ, Savino PJ, Orr LS. Neuroophthalmological complications of enlargement of the third ventricle. Br J Ophthalmol 1978;62:536-42. Palmieri A, Pasquini U, Menichelli F, Salvolini U. Cerebral damage following ventricular shunt for infantile hydrocephalus evaluated by computed tomography. Neuroradiology 1981 ;21 :33-5. Sayers MP. Shunt complications. Clin Neurosurg 1976;23:393400. Sinclair AHH, Dott NM. Hydrocephalus simulating tumor in the production of chiasmal and other parahypophysial lesions. Trans Ophthal Soc UK 1931;51:232-46. Weinberger LM, Webster JE. Visual field defects associated with cerebellar tumors. Arch Ophthalmol 1941;25:128-38.