Chronic Subdural Hematoma Presentingas Transient Neurologic Deficits

JOSEPH E. WELSH, M.D., GEORGE W. TYSON, M.D.,

H. RICHARD WINN, M.D., AND JOHN A. JANE, M.D., PH.D.

SUMMARY Four patients with symptoms of transient neurological dysfunction were subsequently found tohave chronic subdural hematomas (CSDH). The frequency of these episodes diminished significantly afterevacuation of the hematoma. The effects of vascular compromise due to the CSDH and to cardiovascularevents, more commonly implicated in transient ischemic attacks (TIAs) may be additive. The inclusion of acomputerized axial tomographic (CAT) scan in the evaluation of some patients with presumed TIAs isrecommended.

Stroke Vol 10, No 5, 1979

ALTHOUGH chronic subdural hematomas (CSDH)present in a protean fashion, they are rarely confusedwith TIAs.15 The fluctuating signs and symptoms ofCSDH, seen in a significant percentage of patients,6

are usually superimposed on lesser persistentneurologic deficits. In contrast, the definition of a TIAnecessitates complete resolution of symptoms betweenepisodes of vascular insufficiency.7 We have recentlyencountered 4 patients whose presentation was typicalof TIAs, but, who, on further evaluation, were foundto have CSDHs. After the CSDHs were evacuated,their symptoms ceased. The advent of aspirin therapyfor TIAs, contra-indicated in CSDHs, promptedpresentation of the following patients.

Case Reports

Patient 1

Six months prior to admission, a right-handed 53-year-old man experienced abrupt onset of difficultytalking and right arm weakness. These symptomsresolved after 30 min. On the day prior to admission,the patient had 3 similar episodes. The only history ofhead trauma was a cerebral concussion sustained 16years before.

Examination disclosed a mild expressive dysphasiaand right upper extremity paresis. Carotid pulses werestrong and symmetric and there were no bruits.Precordial examination was normal. No retinal em-boli were seen. Hemoglobin, white blood cell count,electrolytes, urinalysis, electrocardiogram, and skullradiographs were normal. A technetium brain scanshowed increased uptake over the left convexity.Bifrontal and left posterior parietal burr holes wereplaced. Thick external membranes were encounteredand a large left-sided chronic subdural hematoma wasdrained. The patient was asymptomatic for the next 18months, but then had a 20 min episode of expressivedysphasia. General physical and neurologic ex-aminations performed shortly after the attack werenormal, as was a CAT scan. For the past 12 months hehas had no further episodes of transient neurologicdysfunction.

From the Department of Neurosurgery, University of Virginia,Charlottesville, VA 22908.

Patient 2

A right-handed 80-year-old woman experiencedmultiple 5-10 min attacks of difficulty talking andwriting over a 4-day period. She was admitted afterthese symptoms had persisted for 24 h. Two monthsbefore, she had transiently lost consciousness during amotor vehicle accident.

During her admission examination, the patient hada 10 min episode of global dysphasia. Carotid pulseswere symmetric and without bruits. Examination wasotherwise unremarkable except for a right sixth nervepalsy, which had been present since her automobile ac-cident. Directional Doppler showed adequateantegrade flow in both ophthalmic arteries. Lumbarpuncture was normal except for a cerebrospinal fluidprotein of 64 mg%. Bilateral carotid angiographydemonstrated a left fronto-parietal subduralhematoma but no stenotic or ulcerated lesions of thecervical or intracranial portions of the internal carotidarteries (fig. la, lb, lc). A chronic subduralhematoma was evacuated through left frontal andposterior parietal burr holes. On the seventhpostoperative day, the patient became abruptlydysphasic. Immediate re-opening of the burr holesrevealed a small reaccumulation of the hematoma.Following evacuation, her symptoms initially im-proved. During the next 24 h, she had multipleepisodes of global dysphasia. A left fronto-parietalcraniotomy disclosed a large, gelatinous subduralhematoma. Two days later, the patient again becamedysphasic. Another small subdural hematoma wasevacuated, the overlying dura was excised, and thebone flap removed. The patient has been asymp-tomatic for 18 months.

Patient 3:

Three months prior to admission, a 73-year-oldright-handed, hypertensive man became dizzy andthen lost consciousness. A second episode 2 monthslater was accompanied by urinary and fecal incon-tinence. During the week prior to admission, he had 4episodes of transient difficulty talking.

Physical examination revealed bilateral soft carotidbruits, a grade III/VI mid systolic murmur, and amild right lower facial paresis. Lumbar punctureshowed 20 red blood cells/mm3 and a protein of 118

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CHRONIC SUBDURAL HEMATOMA/fKe&A el at. 565

FIGURE la (Patient 2): An anteroposterior view ofa trans-femoral left carotid injection. Left-to-right shift of theanterior cerebral arteries, in addition to a left convexitymass, is apparent.

mg/dl. A CAT scan demonstrated a subduralhematoma over the left fronto-parietal convexity (fig.2a, 2b). Thick membranes were found beneath leftfrontal and posterior parietal burr holes. A smallquantity of subdural fluid was evacuated.Postoperatively, loss of vibratory sensation andastereognosis on the right side prompted furtherstudies. A repeat CAT scan was normal. An elec-troencephalogram showed scattered infrequent slowwaves over the left convexity. The signs of parietallobe dysfunction gradually resolved and the patienthas been asymptomatic for 20 months.

Patient 4:

An 81-year-old right-handed male physician wasadmitted following several 10-30 min episodes ofdifficulty talking, accompanied by tingling andweakness in the left upper extremity. Similar symp-toms had occurred 2 weeks prior to admission. Thepatient had chronic hypertension and intermittentclaudication. Additionally, he had been treated withCoumadin after 2 myocardial infarctions.

Admission examination demonstrated a milddysarthria and a left hemiparesis and hemihypalgesia.Bilateral carotid bruits and a 11/VI systolic ejectionmurmur were noted. Repeat neurological examination2 hours after admission was normal. Skullradiographs showed a 4 mm shift of the pineal glandfrom left to right. Brain scan demonstrated increaseduptake over the right fronto-parietal convexity andpossibly over the left parietal convexity as well (fig. 3).

FIGURE lb (Patient 2): A later phase ofthe angiogram seenin fig. la clearly delineates the mass.

The prothrombin time was 24 seconds (control = 11.5seconds). The patient was given intramuscular vitaminK and also fresh frozen plasma. Bilateral frontal andposterior parietal burr holes revealed a right chronicsubdural hematoma and a left subdural hygroma. Per-cutaneous aspiration of the subdural space was per-formed postoperatively because of a persistent mildleft upper extremity paresis and hypalgesia. Nofurther hematoma was evacuated. Gradual, but

FIGURE lc (Patient 2): A lateral view of the left carotid in-jection to show the absence ofintra- or extracranial vasculardisease.

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S66 STROKE VOL 10, No 5, SEPTEMBER-OCTOBER 1979

FIGURE 2a (Patient 3): An unenhanced CAT scan cutthrough the body of the lateral ventricles shows a left extra-cerebral fluid collection.

significant, neurologic improvement was noted duringhis subsequent hospitalization. He was discharged onthe 9th postoperative day with only minor weakness inhis left arm. He has been asymptomatic over the en-suing 4 years.

Discussion

Unlike most patients with CSDHs who present withimpairment of level of consciousness and/or menta-tion, our patients showed only transient signs of focalcerebral dysfunction. In 1733, Schwenke gave the firstdescription of this phenomenon.8 Review of our ownand 6 other reported cases (table) show that dysphasiais almost always part of the presentation. Loeb founddysphasia in 62% of patients with TIAs. HoweverMcKissock10 reported dysphasia in only 18% of hispatients with CSDHs.

Transient neurologic dysfunction has been reportedwith extracerebral masses, although the pathophysi-ology remains unclear.1"-11U Melamud2 suggested 3possibilities: 1) compression of vessels subjacent to the

FIGURE 2b (Patient 3): A higher cut of the CAT scan seenin fig. 2a showing the upper extent of the left convexity fluid.

hematoma, 2) post-ictal cortical suppression, and 3)spreading cortical depression after mechanicalstimulation of the cortex. McLaurin18 postulated thatneurologic deterioration in patients with chronic sub-dural hematomas is sometimes due to increases inregional cerebral edema and not to hematomaenlargement. He also demonstrated that minorchanges in vascular displacement are sometimes ac-companied by major changes in clinical signs andsymptoms. Therefore, a transient increase in regionalswelling may cause a critical degree of vascular dis-placement and consequent ischemia. The focality andtransience of the symptoms may be due to localdifferences in both venous and arterial collateral cir-culation.

We cannot exclude the possibility that these pa-tients with CSDHs had coincidental TIAs. However,the fact that symptoms did not recur in 3 of 4 patientsafter evacuation of the CSDH suggests a causalrelationship.

Regional cerebral blood flow (rCBF) measurementsin areas adjacent to CSDHs have not been performed.A diffuse hemispheric decrease in flow has been noted

Ant L Lat R.Lat Post

P A P L

FIGURE 3 (Patient 4): The late sequence of atechnetium brain scan showing increased up-take over the right and possibly left parietalconvexities.

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CHRONIC SUBDURAL HEMATOMA/WeM et al. 567

TABLE Summary of Published Cases of CSDHs Presenting as Transient Neurologic Deficits

Patients Age Cause of CSDH Presenting signs and symptomsFollow-up:

Duration and neurologic status

Case 1

Case 2

Case 3

Case 4

Groch1

Melamud2

Okihiro3

Robin4

Endtz8

53

80

73

81

59

59

44

64

65

?

Unknown

Head injury with6th nerve palsy2 months PTA

Unknown

Coumadin

Head injury2 weeks PTA

Unknown

Head injury6 weeks PTA

Head injury

Head injury

Head injury

Expressive dysphasia, rightupper extremity paresis

Expressive dysphasia

Expressive dysphasia, rightlower facial paresis,incontinence

Dysarthria, left hemiparesisand hemihypalgesia

Global dysphasia, righthemiparesis

Expressive dysphasia, righthand paresthesias

Expressive dysphasia, righthand paresthesias

Post-CSDH evacuation;expressive dysphasia, rightupper extremity and facialparesis

Post-CSDH evacuation;expressive dysphasia, righthemiparesis

Dysphasia, right hemiparesis,amaurosis, drop attacks

3 years: one episode oftransient dysphasia

13^ years: Asymptomatic

2 years: Asymptomatic

4 years: persistent mild leftupper extremity paresis

Postoperative recovery

6 months: Asymptomatic

Postoperative recovery

Complete recovery after asecond evacuation

Spontaneous resolution

Death: autopsy verificationof a chronic hygroma

by Brodersen,16 but the finding was thought to besecondary to reduced metabolic demand and notischemia. CSDHs may cause a noncritical decrease inrCBF that lowers the threshold for regional ischemiadue to global decreases in CBF or to regional emboli.The effects of CSDH and cardiovascular phenomenaresponsible for transient cerebral ischemia may thusbe additive, with neither alone causing a criticaldecrease in rCBF.

Barnett17 has recently demonstrated that aspirintherapy decreases the incidence of TIAs in somegroups of men. However, any type of anticoagulanttherapy is contra-indicated in patients with a CSDHbecause such treatment may encourage hemorrhagefrom the hematoma capsule. Weisberg6 reported thatthe incidence of unsuspected intracranial structurallesions may be as high as 15% in patients who arethought to have TIAs. We therefore recommend thata CAT scan be considered in all patients withsuspected TIAs before instituting any type of anti-coagulation therapy. SDHs that appear isodense onCAT scan may suggest an improper diagnosis.However, with continuous infusion contrast enhance-ment and careful review of the lateral ventricular con-tour most of these cases can be solved.18

References

1. Groch SN, Hurwitz LJ, Wright IS: Intracranial lesionssimulating cerebral thrombosis. JAMA 172: 1469-1472, 1968

2. Melamud E, Lavy S, Reches A, Sabar A: Chronic subduralhematoma simulating transient ischemic attacks. J Neurosurg42: 101-103, 1975

3. Okihiro MM, Daly D, Yoss RE: Intermittent aphasia due tomass intracranial lesions. Proc Staff Meet Mayo Clin 36:

525-529, 19614. Robin JJ, Maxwell JA, Pitkethly DT: Chronic subdural

hematoma simulating transient ischemic attacks. Ann Neurol4: 154, 1978

5. Weisberg LA, Nice CN: Intracranial tumors simulating thepresentation of cerebrovascular syndromes. Early detectionwith cerebral computed tomography. Am J Med 63: 517-524,1977

6. Cameraon MM: Chronic subdural hematoma: A review of 114cases. Jr Neurol Neurosurg Psychiatry 41: 834-839, 1978

7. Toole JE, Cole M: Ischemic cerebrovascular disease. In BakerAB, Baker CH (eds): Clinical Neurology, Volume 1,Hagerstown, Harper and Row, 1977, p 10

8. Endtz LJ: Historical Article. Post-traumatic hygroma in theEighteenth Century. Described by Thomas Schwenke. SurgNeurol 10: 305-307, 1978

9. Loeb C, Priano A, Albano L: Clinical features and long termfollow-up of patient with reversible ischemic attacks. ActaNeurol Scand 57: 471-480, 1978

10. McKissock W, Richardson A, Bloom W: Subdural hematoma.A review of 389 cases. Lancet I: 1365-1370, 1960

11. Daley DD, Svien JH, Yoss RE: Intermittent cerebral symp-toms with meningiomas. Arch Neurol 5: 287-293, 1961

12. Fincham RW, Worrell JB: Remitting signs in cerebral masslesions. Am Fam Phys 7: 96-100, 1973

13. Fowler GW: Meningioma and intermittent aphasia of 44 yearsduration. J Neurosurg 33: 100-102, 1970

14. Raskind R, Weiss S: Pathologic diagnosis of stroke. Angiology20: 224-235, 1969

15. McLaurin RL: Contributions of angiography to thepathophysiology of subdural hematomas. Neurology(Minneap) 15: 866-873, 1965

16. Brodersen P, Gjerris F: Regional cerebral blood flow in pa-tients with chronic subdural hematomas. Acta Neurol Scand51: 238-239, 1975

17. Barnett HJM, McDonald JWD, Sockett DL: Aspirin—effec-tive in males threatened with stroke. Stroke 9: 295-298, 1978

18. Tsai FY, Huprich JE, Segall HD, Teal JS: The contrast-enhanced CT scan in the diagnosis of isodense subduralhematoma. J Neurosurg 50: 64-69, 1979

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J E Welsh, G W Tyson, H R Winn and J A JaneChronic subdural hematoma presenting as transient neurologic deficits.

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1979 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Stroke doi: 10.1161/01.STR.10.5.564

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