Transient Neurologic Deficit Caused by Chronic Subdural Hematoma HENRYJ. KAMINSKI, M.D., MARYL. HLAVIN, M.D., MATTJ. LIKAVEC,M.D., JAMESW. SCHMIDLEY,M.D., Cleveland, Ohio
R
Transient neurologic deficits are an unusual presentation of chronic subdural hematoma. Presented herein are three patients with transient aphasia and right-sided sensory-motor abnormalities caused by subdural hematoma. Review of the literature revealed 32 cases similar to ours. Presenting complaints were aphasia (77%), sensory symptoms (57%), headache (48%), hemiparesis (50%), and visual disturbance (3%). Fifteen patients underwent cerebral angiography; only three showed significant carotid atherosclerosis. Electroencephalograms were performed in seven patients; five revealed lateralized slowing, but none showed epileptiform activity. Drainage of the hematoma was uniformly curative, although six patients had transient postoperative symptoms. Patients presenting with transient deficits require imaging to rule out the presence of a chronic subdural hematoma.
ecent, retrospective reviews [1,2] of patients with subdural hematoma have not recognized transient neurologic deficits as a sign of chronic subdural hematoma; however, this presentation is probably not rare. Over the course of 9 months, we saw three such cases. Moster et al [3] estimated a 9% incidence of transient neurologic signs or symptoms in patients with chronic subdural hematomas. Recognition of subdural hematoma as a cause of neurologic deficit is of paramount importance, not only because of its favorable response to surgical treatment, but even more so because of the disastrous consequences that may occur if thrombolytic, anticoagulant, or antiplatelet therapy is begun for presumed cerebral ischemia. To increase awareness and understanding of this entity, we present three new cases and review the literature.
CASE REPORTS Patient 1 A 57-year-old right-handed man with adult-onset diabetes mellitus, hypertension, hyperlipidemia, and a remote history of myocardial infarction presented with a a-hour episode of slurred speech, numbness of his right hand and face, incoordination of his right hand, and unsteady gait. Three weeks prior to admission, he had experienced an acute, severe left frontotemporal headache with isolated neck stiffness in its wake. Cardiac murmurs, carotid bruits, and nuchal rigidity were not present. Neurologic examination was normal except for decreased pin and temperature sensation on the left side, including the face, and an unsteady gait. Computed tomographic scans without intravenous contrast were interpreted as normal. Spinal fluid opening pressure was 294 mm HzO. The fluid was xanthochromic, with a protein level of 68 mg/dL and eight red blood cells/mm3. On the second hospital day, cerebral angiography showed minimal irregularities of both carotid bifurcations and displacement of the left hemisphere cortical vessels away from the calvarium, indicative of a subdural mass. During the procedure, the patient developed a right hemiparesis and global aphasia. These neurologic deficits cleared over several hours. Following angiography, an echocardiogram was normal, an elec-
From the Department of Neurology (HJK, JWS), Department of Neurosurgery (MLH, MJL). MetroHealth Medical Center, Cleveland Veterans Affairs Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio. Presented in part at the 42nd Annual Meeting of the American Academy of Neurology, Miami, April 1990. Requests for reprints should be addressed to Henry J. Kaminski, M.D., Department of Neurology 127W, Cleveland Veterans Affairs Medical Center, 10701 East Boulevard, Cleveland, Ohio 44106. Manuscript submitted October 20. 1990, and accepted in revised form March 18, 1991.
698
June
1992
The American
Journal
of Medicine
Volume
92
TRANSIENT
troencephalogram showed left temporal slowing, and repeated computed tomography clearly demonstrated a left frontoparietal subdural hematoma of mixed densities. Drainage was performed through a burr hole. After 1 year, the patient remains asymptomatic.
Patient 3 An 83-year-old man with hypertension, prostate cancer, minor head trauma, and bilateral chronic subdural hematomas thought to be asymptomatic 4 weeks earlier presented with right arm numbness and weakness associated with word-finding difficulties. Physical examination showed mild right hemiparesis and anomia. Computed tomography of the head showed a large, right frontoparieto-occipital subdural hematoma and a smaller left frontoparietal hematoma. During 6 days of observation, he was noted to have three episodes, lasting 5 to 30 minutes, of right hemiparesis and aphasia, two of which occurred while he had therapeutic blood levels of phenytoin. An electroencephalogram showed slowing of the dominant rhythm into the 0 range over the left hemisphere with further intermittent slowing in the left temporal area. He underwent drainage of both hematomas through burr holes. The day after drainage, the patient had right partial motor seizures with post-ictal aphasia. Seizures were controlled with phenytoin. One month later, he was readmitted with a generalized tonic clonic seizure and treated with additional phenytoin.
AND SUBDURAL
HEMATOMA
/ KAMINSKI
ET AL
TABLE I Clinical Characteristicsand InvestigativeStudies Total cases
35
27-87
Age range (years) Male to female ratio
2.51 67
Mean age (years) History of trauma
Patient 2 An %&year-old man with hypertension, aortic insufficiency, and previous atria1 fibrillation presented with complaints of intermittent right-hand weakness over the course of 1 week. One episode had lasted 30 minutes with an associated inability to speak but normal comprehension. Physical examination revealed numerous petechiae and a wellhealed left occipital scar. There was active bleeding of the lips. The neurologic examination was remarkable for a mild left supranuclear facial paresis and mild right pronator drift. The platelet count was 36,000/mm3. The patient was thought to have quinidine-induced thrombocytopenia. Computed tomography of the head showed a chronic left frontoparietal subdural hematoma with effacement of the third and fourth ventricles. When adequate platelet counts were achieved, the patient underwent burr hole drainage of the subdural hematoma. He remained asymptomatic during hospitalization. One year later, he remains asymptomatic, and the results of his neurologic examination have returned to normal.
DEFICIT
20
Manifestations (n = 35) Aphasia
27 (77%) 20 (57%)
Weakness Sensory
20 (57%) 16 (48%)
Headache Visual
1(3%)
Subdural location (n = 35) Left Right
27 (77%) 4 (11%) 4 (11%)
Bilateral EEG (n = 7) Lateralized slowing Epileptiform discharges
5 0
Angiography (n = 15) Extracranial atherosclerosis Mass effect secondary to subdural hematoma
3 15
EfCG= electroencephalogram.
REVIEWOF THE LITERATURE Literature review identified 32 patients [3-81. Reports were reviewed regarding clinical presentation, imaging, electroencephalography, and spinal fluid studies. The results, including those of the current cases, are summarized in Table I. Information in reports was insufficient to estimate the average length of transient neurologic deficits. Eleven patients had deficits on presentation, 11 were normal, and, in the remainder, examination findings were not clearly stated. Only six patients had spinal fluid analysis. The most common abnormality was an elevated protein level (range: 64 to 120 mg/dL). One patient had a completely normal spinal fluid analysis.
COMMENTS Several mechanisms have been postulated for the occurrence of transient deficits secondary to chronic subdural hematomas [3,6]. Common causes of transient ischemic attacks are unlikely to account for the transient findings in the reported patients. Few have had significant cerebrovascular disease by angiography, or heart disease. A review of the literature (Table I) fails to support an epileptic etiology, either by a post-ictal paralysis or specific discharges. The seizures complicating the case of Pa-
June
1992
The American
Journal
of Medicine
Volume
92
699
TRANSIENT
DEFICIT
AND SUBDURAL
HEMATOMA
/ KAMINSKI
ET AL
tient 3 are atypical in this regard. Spreading depression of Leao has also been considered as an etiology [3]. McLaurin [9] recognized that subdural hematomas may compromise regional cerebral blood flow by indirectly shifting the anterior and posterior cerebral arteries. Variations in perfusion pressure, by changes in systemic blood or spinal fluid pressure, could then lead to episodic ischemia. Direct compression may lead to ischemia of the brain beneath the hematoma. The size of the hematoma, however, does not necessarily determine symptoms, nor have most of the reported patients had major degrees of midline shift or syndromes suggesting anterior or posterior cerebral artery ischemia. Our first patient had a small hematoma that was not clearly visible on the initial computed tomographic scan. The cause of his left hemisensory loss is not clear. His hematoma would not be expected to cause a shift of intracranial structures leading to contralateral compression of sensory pathways, and he had no evidence of right hemispheric infarction. The manifestations of headache and sensory and motor disturbances are typical of chronic subdural hematomas, while only 18% of patients in one recent study experienced aphasia [l]. In contrast, 75% of patients with transient symptoms had aphasia. The type of aphasia could not be precisely categorized from our review. Articulatory disturbances and less commonly comprehension abnormalities are described, suggesting greater frontal lobe dysfunction. Poorly localizing word-finding difficulties are also reported. An absence of headache or a history of trauma should not dissuade physicians from considering the diagnosis of chronic subdural hematoma in patients with transient neurologic symptoms. The duration of the neurologic deficit
700
June
1992
The American
Journal
of Medicine
Volume
92
may suggest the presence of a subdural hematoma. It was impossible to estimate the average length of the neurologic deficit by reviewing the literature. The mean length of the deficit in the series reported by Moster et al [3] and in all three of our patients was longer than that of the typical transient ischemit attack [lo]. Anticoagulant or antiplatelet therapy should not be instituted until appropriate imaging has been performed. However, our first patient illustrates the importance of adequate imaging. In the majority of patients, plain computed tomography should be sufficient. In patients with transient neurologic findings unexplained by noncontrasted computed tomography, particularly with prolonged deficit, aphasia, and headache, contrasted computed tomography, magnetic resonance imaging, or angiography should be performed prior to beginning therapy.
REFERENCES 1. Cameron
M. Chronic subdural hematoma: a review of 114 cases. J Neurol Neurosurg Psychiatry 1978; 41: 834-9. 2. Luxon L. Harrison M. Chronic subdural hematoma. Q J Med 1979; 48: 43-53. 3. Moster M, Johnston D, Reinmuth 0. Chronic subdural hematoma with transient neurological deficits: a review of 15 cases. Ann Neurol 1983; 14: 539-42. 4. Lauarino L, Nicolai A, Valassi F. Subacute subdural hematoma presenting as reversible ischemic attacks. ltal J Neurol Sci 1989; 10: 101-3. 5. Robin J, Maxwell J, Pitkethly D. Chronic subdural hematoma simulating transient ischemic attacks [letter]. Ann Neurol 1978; 4: 154. 6. Ross R. Transient tumor attacks. Arch Neurol 1983; 40: 633-6. 7. Russell N, Goumnerova L, Atack E, Atack D, Benoit B. Chronic subdural hematoma mimicking transient ischemic attacks. J Trauma 1985; 25: 1113-4. 8. Zollinger R, Gross R. Traumatic subdural hematoma: an explanation of the late onset of pressure symptoms. JAMA 1934; 103: 245-9. 9. Mclaurin R. Contributions of angiography to the pathophysiology of subdural hematomas. Neurology 1965; 15: 866-73. 10. Levy D. How transient are transient ischemic attacks? Neurology 1988; 38: 674-7.
R
Transient neurologic deficits are an unusual presentation of chronic subdural hematoma. Presented herein are three patients with transient aphasia and right-sided sensory-motor abnormalities caused by subdural hematoma. Review of the literature revealed 32 cases similar to ours. Presenting complaints were aphasia (77%), sensory symptoms (57%), headache (48%), hemiparesis (50%), and visual disturbance (3%). Fifteen patients underwent cerebral angiography; only three showed significant carotid atherosclerosis. Electroencephalograms were performed in seven patients; five revealed lateralized slowing, but none showed epileptiform activity. Drainage of the hematoma was uniformly curative, although six patients had transient postoperative symptoms. Patients presenting with transient deficits require imaging to rule out the presence of a chronic subdural hematoma.
ecent, retrospective reviews [1,2] of patients with subdural hematoma have not recognized transient neurologic deficits as a sign of chronic subdural hematoma; however, this presentation is probably not rare. Over the course of 9 months, we saw three such cases. Moster et al [3] estimated a 9% incidence of transient neurologic signs or symptoms in patients with chronic subdural hematomas. Recognition of subdural hematoma as a cause of neurologic deficit is of paramount importance, not only because of its favorable response to surgical treatment, but even more so because of the disastrous consequences that may occur if thrombolytic, anticoagulant, or antiplatelet therapy is begun for presumed cerebral ischemia. To increase awareness and understanding of this entity, we present three new cases and review the literature.
CASE REPORTS Patient 1 A 57-year-old right-handed man with adult-onset diabetes mellitus, hypertension, hyperlipidemia, and a remote history of myocardial infarction presented with a a-hour episode of slurred speech, numbness of his right hand and face, incoordination of his right hand, and unsteady gait. Three weeks prior to admission, he had experienced an acute, severe left frontotemporal headache with isolated neck stiffness in its wake. Cardiac murmurs, carotid bruits, and nuchal rigidity were not present. Neurologic examination was normal except for decreased pin and temperature sensation on the left side, including the face, and an unsteady gait. Computed tomographic scans without intravenous contrast were interpreted as normal. Spinal fluid opening pressure was 294 mm HzO. The fluid was xanthochromic, with a protein level of 68 mg/dL and eight red blood cells/mm3. On the second hospital day, cerebral angiography showed minimal irregularities of both carotid bifurcations and displacement of the left hemisphere cortical vessels away from the calvarium, indicative of a subdural mass. During the procedure, the patient developed a right hemiparesis and global aphasia. These neurologic deficits cleared over several hours. Following angiography, an echocardiogram was normal, an elec-
From the Department of Neurology (HJK, JWS), Department of Neurosurgery (MLH, MJL). MetroHealth Medical Center, Cleveland Veterans Affairs Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio. Presented in part at the 42nd Annual Meeting of the American Academy of Neurology, Miami, April 1990. Requests for reprints should be addressed to Henry J. Kaminski, M.D., Department of Neurology 127W, Cleveland Veterans Affairs Medical Center, 10701 East Boulevard, Cleveland, Ohio 44106. Manuscript submitted October 20. 1990, and accepted in revised form March 18, 1991.
698
June
1992
The American
Journal
of Medicine
Volume
92
TRANSIENT
troencephalogram showed left temporal slowing, and repeated computed tomography clearly demonstrated a left frontoparietal subdural hematoma of mixed densities. Drainage was performed through a burr hole. After 1 year, the patient remains asymptomatic.
Patient 3 An 83-year-old man with hypertension, prostate cancer, minor head trauma, and bilateral chronic subdural hematomas thought to be asymptomatic 4 weeks earlier presented with right arm numbness and weakness associated with word-finding difficulties. Physical examination showed mild right hemiparesis and anomia. Computed tomography of the head showed a large, right frontoparieto-occipital subdural hematoma and a smaller left frontoparietal hematoma. During 6 days of observation, he was noted to have three episodes, lasting 5 to 30 minutes, of right hemiparesis and aphasia, two of which occurred while he had therapeutic blood levels of phenytoin. An electroencephalogram showed slowing of the dominant rhythm into the 0 range over the left hemisphere with further intermittent slowing in the left temporal area. He underwent drainage of both hematomas through burr holes. The day after drainage, the patient had right partial motor seizures with post-ictal aphasia. Seizures were controlled with phenytoin. One month later, he was readmitted with a generalized tonic clonic seizure and treated with additional phenytoin.
AND SUBDURAL
HEMATOMA
/ KAMINSKI
ET AL
TABLE I Clinical Characteristicsand InvestigativeStudies Total cases
35
27-87
Age range (years) Male to female ratio
2.51 67
Mean age (years) History of trauma
Patient 2 An %&year-old man with hypertension, aortic insufficiency, and previous atria1 fibrillation presented with complaints of intermittent right-hand weakness over the course of 1 week. One episode had lasted 30 minutes with an associated inability to speak but normal comprehension. Physical examination revealed numerous petechiae and a wellhealed left occipital scar. There was active bleeding of the lips. The neurologic examination was remarkable for a mild left supranuclear facial paresis and mild right pronator drift. The platelet count was 36,000/mm3. The patient was thought to have quinidine-induced thrombocytopenia. Computed tomography of the head showed a chronic left frontoparietal subdural hematoma with effacement of the third and fourth ventricles. When adequate platelet counts were achieved, the patient underwent burr hole drainage of the subdural hematoma. He remained asymptomatic during hospitalization. One year later, he remains asymptomatic, and the results of his neurologic examination have returned to normal.
DEFICIT
20
Manifestations (n = 35) Aphasia
27 (77%) 20 (57%)
Weakness Sensory
20 (57%) 16 (48%)
Headache Visual
1(3%)
Subdural location (n = 35) Left Right
27 (77%) 4 (11%) 4 (11%)
Bilateral EEG (n = 7) Lateralized slowing Epileptiform discharges
5 0
Angiography (n = 15) Extracranial atherosclerosis Mass effect secondary to subdural hematoma
3 15
EfCG= electroencephalogram.
REVIEWOF THE LITERATURE Literature review identified 32 patients [3-81. Reports were reviewed regarding clinical presentation, imaging, electroencephalography, and spinal fluid studies. The results, including those of the current cases, are summarized in Table I. Information in reports was insufficient to estimate the average length of transient neurologic deficits. Eleven patients had deficits on presentation, 11 were normal, and, in the remainder, examination findings were not clearly stated. Only six patients had spinal fluid analysis. The most common abnormality was an elevated protein level (range: 64 to 120 mg/dL). One patient had a completely normal spinal fluid analysis.
COMMENTS Several mechanisms have been postulated for the occurrence of transient deficits secondary to chronic subdural hematomas [3,6]. Common causes of transient ischemic attacks are unlikely to account for the transient findings in the reported patients. Few have had significant cerebrovascular disease by angiography, or heart disease. A review of the literature (Table I) fails to support an epileptic etiology, either by a post-ictal paralysis or specific discharges. The seizures complicating the case of Pa-
June
1992
The American
Journal
of Medicine
Volume
92
699
TRANSIENT
DEFICIT
AND SUBDURAL
HEMATOMA
/ KAMINSKI
ET AL
tient 3 are atypical in this regard. Spreading depression of Leao has also been considered as an etiology [3]. McLaurin [9] recognized that subdural hematomas may compromise regional cerebral blood flow by indirectly shifting the anterior and posterior cerebral arteries. Variations in perfusion pressure, by changes in systemic blood or spinal fluid pressure, could then lead to episodic ischemia. Direct compression may lead to ischemia of the brain beneath the hematoma. The size of the hematoma, however, does not necessarily determine symptoms, nor have most of the reported patients had major degrees of midline shift or syndromes suggesting anterior or posterior cerebral artery ischemia. Our first patient had a small hematoma that was not clearly visible on the initial computed tomographic scan. The cause of his left hemisensory loss is not clear. His hematoma would not be expected to cause a shift of intracranial structures leading to contralateral compression of sensory pathways, and he had no evidence of right hemispheric infarction. The manifestations of headache and sensory and motor disturbances are typical of chronic subdural hematomas, while only 18% of patients in one recent study experienced aphasia [l]. In contrast, 75% of patients with transient symptoms had aphasia. The type of aphasia could not be precisely categorized from our review. Articulatory disturbances and less commonly comprehension abnormalities are described, suggesting greater frontal lobe dysfunction. Poorly localizing word-finding difficulties are also reported. An absence of headache or a history of trauma should not dissuade physicians from considering the diagnosis of chronic subdural hematoma in patients with transient neurologic symptoms. The duration of the neurologic deficit
700
June
1992
The American
Journal
of Medicine
Volume
92
may suggest the presence of a subdural hematoma. It was impossible to estimate the average length of the neurologic deficit by reviewing the literature. The mean length of the deficit in the series reported by Moster et al [3] and in all three of our patients was longer than that of the typical transient ischemit attack [lo]. Anticoagulant or antiplatelet therapy should not be instituted until appropriate imaging has been performed. However, our first patient illustrates the importance of adequate imaging. In the majority of patients, plain computed tomography should be sufficient. In patients with transient neurologic findings unexplained by noncontrasted computed tomography, particularly with prolonged deficit, aphasia, and headache, contrasted computed tomography, magnetic resonance imaging, or angiography should be performed prior to beginning therapy.
REFERENCES 1. Cameron
M. Chronic subdural hematoma: a review of 114 cases. J Neurol Neurosurg Psychiatry 1978; 41: 834-9. 2. Luxon L. Harrison M. Chronic subdural hematoma. Q J Med 1979; 48: 43-53. 3. Moster M, Johnston D, Reinmuth 0. Chronic subdural hematoma with transient neurological deficits: a review of 15 cases. Ann Neurol 1983; 14: 539-42. 4. Lauarino L, Nicolai A, Valassi F. Subacute subdural hematoma presenting as reversible ischemic attacks. ltal J Neurol Sci 1989; 10: 101-3. 5. Robin J, Maxwell J, Pitkethly D. Chronic subdural hematoma simulating transient ischemic attacks [letter]. Ann Neurol 1978; 4: 154. 6. Ross R. Transient tumor attacks. Arch Neurol 1983; 40: 633-6. 7. Russell N, Goumnerova L, Atack E, Atack D, Benoit B. Chronic subdural hematoma mimicking transient ischemic attacks. J Trauma 1985; 25: 1113-4. 8. Zollinger R, Gross R. Traumatic subdural hematoma: an explanation of the late onset of pressure symptoms. JAMA 1934; 103: 245-9. 9. Mclaurin R. Contributions of angiography to the pathophysiology of subdural hematomas. Neurology 1965; 15: 866-73. 10. Levy D. How transient are transient ischemic attacks? Neurology 1988; 38: 674-7.
