LETTERS
Transient Spastic Paraparesis Following Abdominal Aortography : Management with Cerebrospinal Fluid Lavage
2. Dardjiev V, Symeonov A, Chankov I: Etiology, pathogenesis, and prevention of spinal cord lesions in selective angiography of the bronchial and intercostal arteries. Radiology 112:81-83, 1974 3. Di Chiro G Unintentional spinal cord arteriography:a warning. Radiology 112:231-233, 1974 4. Killen DA, Foster JH: Spinal cord injury as a complication of aortography. Ann Surg 152:211-230, 1960
Mircea A. Morariu, M D
Immunological Studies Related to Brain Antigens in Huntington’s Disease
Paraplegia following translumbar aortography was described by Antoni and Lindgren [ l ] in 1949, and the pathogenetic mechanisms have recently been reviewed [21. W e examined a man in whom spastic paraparesis developed following an injection of contrast material into the abdominal aorta. A 57-year-old white man was admitted to the hospital for investigation of suspected bilateral carotid stenosis and peripheral vascular disease in the lower extremities. A transaxillary Catheterization was performed. Immediately following the second injection of 35 cc of contrast material (Renografin-76) into the abdominal aorta, the patient developed pain, stiffness, and weakness in both lower limbs. Muscle tone was increased in extensor muscles of both legs, and he was barely able to move those limbs. There were no sensory disturbances. T h e knee and ankle jerks were brisk, and plantar responses were extensor. Approximately 25 minutes after the onset of these neurological disturbances, cerebrospinal fluid lavage was initiated by withdrawing CSF in 10 ml aliquots and replacing it with similar amounts of isotonic saline. I n this manner, 70 ml of CSF was removed within a few minutes. Prior to the lavage the CSF iodine level had been 17,750 pg per deciliter; o n completion o f t h e lavage it was 2,355 pg per deciliter. Ten milligrams of dexamethasone (2.5 ml of Decadron) was also administered intravenously. O n e hour after the onset of paraparesis, spasticity and pain were lessened and motility in the lower limbs had improved. Within two hours the patient was neurologically normal. Conceivably, in this patient contrast material entered intraspinal vessels during the aortography, and its neurotoxicity produced spastic paraparesis. This complication has been attributed to a direct toxic effect of iodine on the spinal cord [2, 41, and D i Chiro [31 has recommended CSF lavage as emergency therapy for postangiographic paraplegia. The initial high level of CSF iodine recorded in our patient and its decline after lavage support the toxicity attributed to iodine as well as the recommended management by CSF lavage. T h e results justify further efforts to treat similar patients with CSF lavage.
Ralph C. Williams, Jr, MD, Mary Lewis, BS, Jean Montatio, BS, Larry E. Davis, MD, and Gunnar Husby, M D W e have studied 10 patients with Huntington’s disease (HD) and 14 control patients with neurological disease as well as 14 normal subjects to determine lymphocyte transformation. The tests were done using 2 X lo5lymphocytes and three concentrations of human brain antigens prepared as water or perchloric acid extracts from glia-enriched or neuron-rich sucrose gradient fractions of cerebral cortex, caudate nucleus, and cerebellum [4]. The extracts were derived from HD brain as well as from control normal brain. All antigen samples were coded and studied singly, blind, without knowledge of their source. In addition, a panel of sera from patients with HD as well as control sera were tested by indirect immunofluorescence against unfixed frozen sections of similar tissues from both HD and normal subjects. Fluorescein-con jugated anti-human IgG and anti-human C3 [2, 31 were used. Clear positive reactivity (stimulation index 3 3) for several antigens extracted from central nervous system material was noted in 7 to 17% of HD patients and in 6 to 15% of neurological controls. Similarly, 2 to 11% of normal controls showed positive stimulation. No significant differences between the HD and other controlgroups was recorded. No preferential reactivity was noted when HD lymphocytes were stimulated with 12 different antigenic preparations derived from HD brain in comparison to 15 preparations from normal brain. When HD caudate nucleus, cerebral cortex, and cerebellum were compared with similar tissues obtained from normal controls, prevalence of positive indirect immunofluorescence reactions for IgG binding to neuronal cytoplasm was similar with HD sera containing IgG antineuronal antibody. Again, no specificity for antigens unique to HD brain was detected. Our data provide no evidence for cell-mediated immune reactivity in HD pa-
References 1. Anroni
N, Lindgren E: Steno’s experiment in man as complica-
tion in lumbar aortography.ActaChir Scand 98:230-247,1949
From the Division of Neurology, Department of Neurology and Neurological Surgery, Henry Ford Hospital, Detroit, MI 48202.
From the Departments of Medicine and Neurology, Bernalillo County Medical Center, University of New Mexico School of
Medicine, Albuquerque, NM. Address reprint requests to Dr Williams, Department of Medicine, University of New Mexico School of Medicine, Albuquerque, N M 87 106.
0364-5 134/78/0003-02 16t01.00 @ 1978 by the American Neurological Association
185
Transient Spastic Paraparesis Following Abdominal Aortography : Management with Cerebrospinal Fluid Lavage
2. Dardjiev V, Symeonov A, Chankov I: Etiology, pathogenesis, and prevention of spinal cord lesions in selective angiography of the bronchial and intercostal arteries. Radiology 112:81-83, 1974 3. Di Chiro G Unintentional spinal cord arteriography:a warning. Radiology 112:231-233, 1974 4. Killen DA, Foster JH: Spinal cord injury as a complication of aortography. Ann Surg 152:211-230, 1960
Mircea A. Morariu, M D
Immunological Studies Related to Brain Antigens in Huntington’s Disease
Paraplegia following translumbar aortography was described by Antoni and Lindgren [ l ] in 1949, and the pathogenetic mechanisms have recently been reviewed [21. W e examined a man in whom spastic paraparesis developed following an injection of contrast material into the abdominal aorta. A 57-year-old white man was admitted to the hospital for investigation of suspected bilateral carotid stenosis and peripheral vascular disease in the lower extremities. A transaxillary Catheterization was performed. Immediately following the second injection of 35 cc of contrast material (Renografin-76) into the abdominal aorta, the patient developed pain, stiffness, and weakness in both lower limbs. Muscle tone was increased in extensor muscles of both legs, and he was barely able to move those limbs. There were no sensory disturbances. T h e knee and ankle jerks were brisk, and plantar responses were extensor. Approximately 25 minutes after the onset of these neurological disturbances, cerebrospinal fluid lavage was initiated by withdrawing CSF in 10 ml aliquots and replacing it with similar amounts of isotonic saline. I n this manner, 70 ml of CSF was removed within a few minutes. Prior to the lavage the CSF iodine level had been 17,750 pg per deciliter; o n completion o f t h e lavage it was 2,355 pg per deciliter. Ten milligrams of dexamethasone (2.5 ml of Decadron) was also administered intravenously. O n e hour after the onset of paraparesis, spasticity and pain were lessened and motility in the lower limbs had improved. Within two hours the patient was neurologically normal. Conceivably, in this patient contrast material entered intraspinal vessels during the aortography, and its neurotoxicity produced spastic paraparesis. This complication has been attributed to a direct toxic effect of iodine on the spinal cord [2, 41, and D i Chiro [31 has recommended CSF lavage as emergency therapy for postangiographic paraplegia. The initial high level of CSF iodine recorded in our patient and its decline after lavage support the toxicity attributed to iodine as well as the recommended management by CSF lavage. T h e results justify further efforts to treat similar patients with CSF lavage.
Ralph C. Williams, Jr, MD, Mary Lewis, BS, Jean Montatio, BS, Larry E. Davis, MD, and Gunnar Husby, M D W e have studied 10 patients with Huntington’s disease (HD) and 14 control patients with neurological disease as well as 14 normal subjects to determine lymphocyte transformation. The tests were done using 2 X lo5lymphocytes and three concentrations of human brain antigens prepared as water or perchloric acid extracts from glia-enriched or neuron-rich sucrose gradient fractions of cerebral cortex, caudate nucleus, and cerebellum [4]. The extracts were derived from HD brain as well as from control normal brain. All antigen samples were coded and studied singly, blind, without knowledge of their source. In addition, a panel of sera from patients with HD as well as control sera were tested by indirect immunofluorescence against unfixed frozen sections of similar tissues from both HD and normal subjects. Fluorescein-con jugated anti-human IgG and anti-human C3 [2, 31 were used. Clear positive reactivity (stimulation index 3 3) for several antigens extracted from central nervous system material was noted in 7 to 17% of HD patients and in 6 to 15% of neurological controls. Similarly, 2 to 11% of normal controls showed positive stimulation. No significant differences between the HD and other controlgroups was recorded. No preferential reactivity was noted when HD lymphocytes were stimulated with 12 different antigenic preparations derived from HD brain in comparison to 15 preparations from normal brain. When HD caudate nucleus, cerebral cortex, and cerebellum were compared with similar tissues obtained from normal controls, prevalence of positive indirect immunofluorescence reactions for IgG binding to neuronal cytoplasm was similar with HD sera containing IgG antineuronal antibody. Again, no specificity for antigens unique to HD brain was detected. Our data provide no evidence for cell-mediated immune reactivity in HD pa-
References 1. Anroni
N, Lindgren E: Steno’s experiment in man as complica-
tion in lumbar aortography.ActaChir Scand 98:230-247,1949
From the Division of Neurology, Department of Neurology and Neurological Surgery, Henry Ford Hospital, Detroit, MI 48202.
From the Departments of Medicine and Neurology, Bernalillo County Medical Center, University of New Mexico School of
Medicine, Albuquerque, NM. Address reprint requests to Dr Williams, Department of Medicine, University of New Mexico School of Medicine, Albuquerque, N M 87 106.
0364-5 134/78/0003-02 16t01.00 @ 1978 by the American Neurological Association
185
