- Email: [email protected]
Thalamic hemorrhage imitating hyperventilation
CASE REPORT hemorrhage, thalamic; hyperventilation
Thalamic Hemorrhage Imitating Hyperventilation A 52-year-old woman developed subjective right hemiparesthesias over a two-day period. Because of a paucity of physical findings, apparent anxiety with tachypnea, and a respiratory alkalosis with hypocapnia, a diagnosis of hyperventilation syndrome was considered. However, because of the unilateral symptoms, a computed tomography scan was performed, demonstrating a left posterior thalamic infarct. Most reports of thalamic infarct indicate altered mental status, vertical gaze palsies, or sensorimotor hemiparesis with sensory involvement predominant. The case of a patient with thalamic hemorrhage who presented with only hemiparesthesia is reported to heighten clinicians' awareness of this diagnosis. [Scialdone AM: Thalamic hemorrhage imitating hyperventilation. Ann Emerg Med July 1990;19:817-819.] INTRODUCTION Many authors believe that isolated thalamic hemorrhages are rare.~ The agreed-on classic presentation of thalamic hemorrhage is the sudden onset of hemiplegia or paresis associated with a hemihypesthesia and altered mental status. 2 However, these symptoms are believed to arise primarily as a result of the involvement of structures adjacent to the thalamus. Clinical studies during the past ten years have shown that the thalamus also plays a role in language and memory. There have been no reports, however, of isolated paresthesia without evidence of dysesthesia or some other impairment of sensory or motor modalities.
Anthony M Scialdone, MD Canton, Ohio From the Department of Emergency Medicine, Timken-Mercy Medical Center, Canton, Ohio. Received for publication August 23, 1989. Revision received December 14, 1989. Accepted for publication January 5, 1990. Address for reprints: Anthony M Scialdone, MD, Department of Emergency Medicine, Doctors Hospital, 1087 Dennison Avenue, Columbus, Ohio 43201-3496.
CASE REPORT A 52-year-old woman presented to the emergency department complaining of tingling of the right side of her body. Her symptoms had begun two days before her presentation with the onset, at rest, of tingling in her right arm, which progressed to involve the right side of the face and the right leg. She noted some nausea during the two days before presentation, with an episode of vomiting the day before. She denied headache, neck stiffness, gait disturbance, weakness, visual disturbance, and speech difficulty. Family members stated that they had not noted any disturbance of affect or intellect. She had no psychiatric history and had not been under any recent stresses. She had a history of hypertension and adult-onset diabetes and was taking atenolol and glyburide. Physical examination revealed a morbidly obese woman with an estimated weight of more than 100 kg. She was alert and oriented. Her blood pressure was 160/80 m m Hg; pulse, 82 and regular; respirations, 40 without retraction; and temperature, 37.4 C. She appeared to be inappropriately anxious with frequent hand-wringing noted. Cranial nerve examination was normal. She had normal speech patterns and no aphasia. Motor examination of both upper and lower extremities was normal. Reflexes were symmetric, and plantar responses were normal. There was no hemisensory deficit to light touch, two-point discrimination, or proprioception. Gait was tested and found to be normal. The thyroid was nonpalpable, and there was no nuchal rigidity. Lungs were clear to auscultation, and the heart was without murmurs or gallops. Laboratory studies revealed WBC of 9,300 with a normal cell differential. Hemoglobin was 14.8. Electrolytes revealed sodium, 138 mEq/L; po-
19:7 July 1990
Annals of Emergency Medicine
817/131
THALAMIC HEMORRHAGE Scialdone
tassium, 3.5 mEq/L; BUN, 13 mg/dL; and blood sugar, 267 mg/dL. A n ECG r e v e a l e d d i f f u s e n o n s p e c i f i c ST-T c h a n g e s . A r t e r i a l b l o o d g a s e s revealed P o a of 99 m m Hg on r o o m air of 99; Pco2, 27 r n m Hg; and pH, 7.56 w i t h H C O 3 of 24 mEqL. C o n s i d e r i n g the p a t i e n t ' s p a u c i t y of clinical findings, her apparent anxiety, and her respiratory alkalosis w i t h h y p o c a r b i a , a diagnosis of hyp e r v e n t i l a t i o n s y n d r o m e was briefly entertained. However, the unilaterali t y of h e r p a r e s t h e s i a s and h e r history of h y p e r t e n s i o n led to the decision to perform a c o m p u t e d tomograp h y (CT) scan of the brain. The scan r e v e a l e d a 1.2-cm c i r c u l a r h e m o r rhage of the left posterior thalamus. The p a t i e n t was a d m i t t e d to the hospital for further evaluation. During a s e v e n - d a y h o s p i t a l i z a t i o n , no f u r t h e r n e u r o l o g i c s e q u e l a e developed, and h e r p a r e s t h e s i a s resolved. Her a n t i h y p e r t e n s i v e m e d i c a t i o n was adjusted, and she was placed on insulin therapy. There have been no further difficulties since the event. DISCUSSION More t h a n 90% of t h a l a m i c insults are h e m o r r h a g i c in n a t u r e and secondary to vascular rupture. There is a high association w i t h h y p e r t e n s i o n J The larger the lesion, the greater the morbidity and mortality; in one study, all lesions m o r e than 3.0 c m were fatal.3, 4 Lesions that limit t h e m s e l v e s to the t h a l a m u s are probably quite rare. In one retrospective study of 7,600 C T scans, only 21 appeared isolated w i t h i n the thalamus; even in those few, the authors admitted that scan could not indicate w h e t h e r the lesion was t r u l y anatomically l i m i t e d to the thalamus. 1 M o s t lesions e x t e n d e d into adjacent structures such as the i n t e r n a l capsule or ventricle. T h e classic p r e s e n t a t i o n of a c u t e thalamic insult was described by Tisher as a p r e d o m i n a n c e of sensory over m o t o r deficits, an altered level of consciousness, disturbance of ocul o m o t o r f u n c t i o n , b i l a t e r a l nonreactive m i o s i s , a n d B a b i n s k i signs.2, 5 This definition has r e m a i n e d essentially u n a l t e r e d since that time. In all r e t r o s p e c t i v e c l i n i c a l studies, h e m i paresis, h e m i h y p e s t h e s i a , and dist u r b e d levels of c o n s c i o u s n e s s have been markedly preponderant. 6 This m a y occur b e c a u s e m o s t l e s i o n s of 132/818
the t h a l a m u s do n o t exert their clinical effects on only the t h a l a m u s but, by extension, also into adjacent structures. It has been p o s t u l a t e d that h e m i paresis is caused by extension of the insult into the internal capsule. Ocular disturbances such as vertical gaze palsies and d o w n w a r d eye deviation are t h o u g h t to develop because of extension into the s u b t h a l a m u s or dorsal midbrain. 7 It also has been diffic u l t to a s s e s s s e n s o r y d e f i c i t s in m a n y p a t i e n t s because of d i m i n i s h e d sensorium. 8 Indeed, the level of consciousness is the m o s t i m p o r t a n t factor in prognosis. 1 D u r i n g the past ten years, reports have i n d i c a t e d the c o m p l e x nature of thalamic function. Stereotactic studies and surgical t h a l a m o t o m i e s have aided in mapping functional roles for d i f f e r e n t s e g m e n t s of t h e t h a l a m u s . L e s i o n s of t h e m e d i a l t h a l a m u s h a v e b e e n i m p l i c a t e d in memory impairment and disturb a n c e s of c o n s c i o u s n e s s . 9 A n t e r o l a t e r a l i n j u r y h a s r e s u l t e d in i m paired verbal m e m o r y , h e m i - i n a t t e n t i o n , a n d n e g l e c t s y n d r o m e s , m~3 A p h a s i a and other types of language d y s f u n c t i o n , such as r e d u c e d voice v o l u m e , p e r s e v e r a t i o n , a n o m i a , and speech arrest, have also been noted in lesions of the d o m i n a n t anterolateral thalamus.5,8,1a, 14-~7 In p o s t e r o l a t e r a l lesions, in w h i c h 76% of all t h a l a m i c h e m o r r h a g e s arise, m o t o r a n d sensory d e f i c i t s p r e d o m i n a t e over prefrontal signs.8,1¢ls, is It has also been d o c u m e n t e d that o c u l o m o t o r disturbances originate from lesions of the posterior thalamus.19, 2o In the previously described patient, the clinical findings were u n u s u a l l y subtle, w i t h no d o c u m e n t a b l e neurologic findings of speech d i s t u r b a n c e or m e m o r y i m p a i r m e n t . N o r w a s there any evidence of sensory, motor, or cranial nerve dysfunction despite independent examination by two emergency physicians. This patient could have been dismissed as having a hyperventilation syndrome and a c u t e a n x i e t y given h e r absence of neurologic findings and a docum e n t e d respiratory alkalosis w i t h o u t hypoxia. H o w e v e r , h y p e r v e n t i l a t i o n was an u n l i k e l y diagnosis because of the u n i l a t e r a l nature of her paresthesias w i t h sparing of the perioral region, a b s e n c e of carpopedal spasm, and lack of psychiatric history. Annals of Emergency Medicine
SUMMARY T h e case of a 52-year-old diabetic and h y p e r t e n s i v e w o m a n w h o presented w i t h c o m p l a i n t s of right sided p a r e s t h e s i a s is r e p o r t e d . She w a s f o u n d to h a v e a t h a l a m i c h e m o r rhage. This case, as well as the brief r e v i e w of p r e v i o u s c l i n i c a l reports, should alert the e m e r g e n c y p h y s i c i a n to consider the possibility of t h a l a m i c insult in any p a t i e n t comp l a i n i n g of hemiparesthesias, particularly older patients w i t h a h i s t o r y of h y p e r t e n s i v e disease. T h e diagnosis should also be considered in patients w i t h speech or m e m o r y i m p a i r m e n t or h e m i - i n a t t e n t i o n s y n d r o m e s , regardless of w h e t h e r clinical evidence of sensory or m o t o r deficit is present.
REFERENCES
1. Piepgras U, Rieger P: Thalamic bleeding: Diagnosis, course, and prognosis. Neuroradiology 1981;22:85-91. 2. Fisher CM: The pathological and clinical aspects of thalamic hemorrhage. Trans A m Neurol Assoc 1959;84:56-59. 3. Barracquer-BordasL, Illa I, Escartin A, et al: Thalamic hemorrhage: A study of 23 patients with diagnosis by computerized tomography. Stroke 1981;12:524-527. 4. Weisberg L: Thalamic hemorrhage: ClinicalCT correlations. Neurology 1986~36:1382q386. 5. Fazio C, Sacco G, Bugiani O, et al: The thalamic hemorrhage: An anatamo-clinical study. Eur Neurol 1973;9:30-43. 6. Goto N, Kaneko M, Muraki M, et al: Thalamic hemorrhage - A clinicoanatomic study. Neurol Med Chir (Tokyo) 1982;22:24-36. 7. Hankey G, Stewart-Wynne E: Anmesia following thalamic hemorrhage. Stroke 1988;19: 776-778. 8. Kawahara N, Sato K, Muraki M, et al: CT classification of thalamic hemorrhages and their clinical implications. Neurology 1986;36: 165-172. 9. Choi D, Sudarsky L~Schacter S, et al: Medial thalamic hemorrhage with amnesia. Arch Neurol 1983~40:611-613. 10. Waxman S, Ricaurte G, Tucker S, et al: Thalamic hemorrhage with neglect and memory disorder. ] Neurol Sci 1986;75:105-112. ll, Santamaria J, BlesaR, Tolosa E, et ah Confnsional syndrome in thalamic stroke. Neurology 1984;34:1618. 12. Maiuri F, Signorella C, Collela G, et al: Aphasia and left thalamic hemorrhage. Clin Neurol Chir 1983~1:20-24. 13. Leiguarda R: Environmental reduplication associated with a right thalamic hemorrhage. [ Neurol Neurosurg Psychiatry 1983;46:1154. 14. Kosten T, Rappaport A: Left thalamic hemorrhage and aphasia. Corm Med 1982;4:633-635. 15. Kirshner H, Kistler K: Aphasia after right thalamic hemorrhage. A r c h N e u r o l 1982 i 39:667-669. 19:7 July 1990
16. C h e s s o n A: A p h a s i a following a right thalamic hemorrhage. Brain Language 1983;19: 306-316.
18. Verma A, Maheshwari M: Hypestheticataxic-hemiparesis in thalamic hemorrhage. Stroke 1986;7:49-51.
17. Ciemens V: Localized thalamic hemorrhage. Neurology 1970;20:776-782.
19. Hirose G, Kosoegawa H, Saeki M, et al: The syndrome of posterior thalamic hemorrhage.
19:7 July 1990
Annals of Emergency Medicine
Neurology 1985;35:998-1002. 20. Hier D, Davis K, Richardson g Jr, et al: Hypertensive putaminal hemorrhage. Ann Neurol 1977;1:152-159.
819/133
Thalamic Hemorrhage Imitating Hyperventilation A 52-year-old woman developed subjective right hemiparesthesias over a two-day period. Because of a paucity of physical findings, apparent anxiety with tachypnea, and a respiratory alkalosis with hypocapnia, a diagnosis of hyperventilation syndrome was considered. However, because of the unilateral symptoms, a computed tomography scan was performed, demonstrating a left posterior thalamic infarct. Most reports of thalamic infarct indicate altered mental status, vertical gaze palsies, or sensorimotor hemiparesis with sensory involvement predominant. The case of a patient with thalamic hemorrhage who presented with only hemiparesthesia is reported to heighten clinicians' awareness of this diagnosis. [Scialdone AM: Thalamic hemorrhage imitating hyperventilation. Ann Emerg Med July 1990;19:817-819.] INTRODUCTION Many authors believe that isolated thalamic hemorrhages are rare.~ The agreed-on classic presentation of thalamic hemorrhage is the sudden onset of hemiplegia or paresis associated with a hemihypesthesia and altered mental status. 2 However, these symptoms are believed to arise primarily as a result of the involvement of structures adjacent to the thalamus. Clinical studies during the past ten years have shown that the thalamus also plays a role in language and memory. There have been no reports, however, of isolated paresthesia without evidence of dysesthesia or some other impairment of sensory or motor modalities.
Anthony M Scialdone, MD Canton, Ohio From the Department of Emergency Medicine, Timken-Mercy Medical Center, Canton, Ohio. Received for publication August 23, 1989. Revision received December 14, 1989. Accepted for publication January 5, 1990. Address for reprints: Anthony M Scialdone, MD, Department of Emergency Medicine, Doctors Hospital, 1087 Dennison Avenue, Columbus, Ohio 43201-3496.
CASE REPORT A 52-year-old woman presented to the emergency department complaining of tingling of the right side of her body. Her symptoms had begun two days before her presentation with the onset, at rest, of tingling in her right arm, which progressed to involve the right side of the face and the right leg. She noted some nausea during the two days before presentation, with an episode of vomiting the day before. She denied headache, neck stiffness, gait disturbance, weakness, visual disturbance, and speech difficulty. Family members stated that they had not noted any disturbance of affect or intellect. She had no psychiatric history and had not been under any recent stresses. She had a history of hypertension and adult-onset diabetes and was taking atenolol and glyburide. Physical examination revealed a morbidly obese woman with an estimated weight of more than 100 kg. She was alert and oriented. Her blood pressure was 160/80 m m Hg; pulse, 82 and regular; respirations, 40 without retraction; and temperature, 37.4 C. She appeared to be inappropriately anxious with frequent hand-wringing noted. Cranial nerve examination was normal. She had normal speech patterns and no aphasia. Motor examination of both upper and lower extremities was normal. Reflexes were symmetric, and plantar responses were normal. There was no hemisensory deficit to light touch, two-point discrimination, or proprioception. Gait was tested and found to be normal. The thyroid was nonpalpable, and there was no nuchal rigidity. Lungs were clear to auscultation, and the heart was without murmurs or gallops. Laboratory studies revealed WBC of 9,300 with a normal cell differential. Hemoglobin was 14.8. Electrolytes revealed sodium, 138 mEq/L; po-
19:7 July 1990
Annals of Emergency Medicine
817/131
THALAMIC HEMORRHAGE Scialdone
tassium, 3.5 mEq/L; BUN, 13 mg/dL; and blood sugar, 267 mg/dL. A n ECG r e v e a l e d d i f f u s e n o n s p e c i f i c ST-T c h a n g e s . A r t e r i a l b l o o d g a s e s revealed P o a of 99 m m Hg on r o o m air of 99; Pco2, 27 r n m Hg; and pH, 7.56 w i t h H C O 3 of 24 mEqL. C o n s i d e r i n g the p a t i e n t ' s p a u c i t y of clinical findings, her apparent anxiety, and her respiratory alkalosis w i t h h y p o c a r b i a , a diagnosis of hyp e r v e n t i l a t i o n s y n d r o m e was briefly entertained. However, the unilaterali t y of h e r p a r e s t h e s i a s and h e r history of h y p e r t e n s i o n led to the decision to perform a c o m p u t e d tomograp h y (CT) scan of the brain. The scan r e v e a l e d a 1.2-cm c i r c u l a r h e m o r rhage of the left posterior thalamus. The p a t i e n t was a d m i t t e d to the hospital for further evaluation. During a s e v e n - d a y h o s p i t a l i z a t i o n , no f u r t h e r n e u r o l o g i c s e q u e l a e developed, and h e r p a r e s t h e s i a s resolved. Her a n t i h y p e r t e n s i v e m e d i c a t i o n was adjusted, and she was placed on insulin therapy. There have been no further difficulties since the event. DISCUSSION More t h a n 90% of t h a l a m i c insults are h e m o r r h a g i c in n a t u r e and secondary to vascular rupture. There is a high association w i t h h y p e r t e n s i o n J The larger the lesion, the greater the morbidity and mortality; in one study, all lesions m o r e than 3.0 c m were fatal.3, 4 Lesions that limit t h e m s e l v e s to the t h a l a m u s are probably quite rare. In one retrospective study of 7,600 C T scans, only 21 appeared isolated w i t h i n the thalamus; even in those few, the authors admitted that scan could not indicate w h e t h e r the lesion was t r u l y anatomically l i m i t e d to the thalamus. 1 M o s t lesions e x t e n d e d into adjacent structures such as the i n t e r n a l capsule or ventricle. T h e classic p r e s e n t a t i o n of a c u t e thalamic insult was described by Tisher as a p r e d o m i n a n c e of sensory over m o t o r deficits, an altered level of consciousness, disturbance of ocul o m o t o r f u n c t i o n , b i l a t e r a l nonreactive m i o s i s , a n d B a b i n s k i signs.2, 5 This definition has r e m a i n e d essentially u n a l t e r e d since that time. In all r e t r o s p e c t i v e c l i n i c a l studies, h e m i paresis, h e m i h y p e s t h e s i a , and dist u r b e d levels of c o n s c i o u s n e s s have been markedly preponderant. 6 This m a y occur b e c a u s e m o s t l e s i o n s of 132/818
the t h a l a m u s do n o t exert their clinical effects on only the t h a l a m u s but, by extension, also into adjacent structures. It has been p o s t u l a t e d that h e m i paresis is caused by extension of the insult into the internal capsule. Ocular disturbances such as vertical gaze palsies and d o w n w a r d eye deviation are t h o u g h t to develop because of extension into the s u b t h a l a m u s or dorsal midbrain. 7 It also has been diffic u l t to a s s e s s s e n s o r y d e f i c i t s in m a n y p a t i e n t s because of d i m i n i s h e d sensorium. 8 Indeed, the level of consciousness is the m o s t i m p o r t a n t factor in prognosis. 1 D u r i n g the past ten years, reports have i n d i c a t e d the c o m p l e x nature of thalamic function. Stereotactic studies and surgical t h a l a m o t o m i e s have aided in mapping functional roles for d i f f e r e n t s e g m e n t s of t h e t h a l a m u s . L e s i o n s of t h e m e d i a l t h a l a m u s h a v e b e e n i m p l i c a t e d in memory impairment and disturb a n c e s of c o n s c i o u s n e s s . 9 A n t e r o l a t e r a l i n j u r y h a s r e s u l t e d in i m paired verbal m e m o r y , h e m i - i n a t t e n t i o n , a n d n e g l e c t s y n d r o m e s , m~3 A p h a s i a and other types of language d y s f u n c t i o n , such as r e d u c e d voice v o l u m e , p e r s e v e r a t i o n , a n o m i a , and speech arrest, have also been noted in lesions of the d o m i n a n t anterolateral thalamus.5,8,1a, 14-~7 In p o s t e r o l a t e r a l lesions, in w h i c h 76% of all t h a l a m i c h e m o r r h a g e s arise, m o t o r a n d sensory d e f i c i t s p r e d o m i n a t e over prefrontal signs.8,1¢ls, is It has also been d o c u m e n t e d that o c u l o m o t o r disturbances originate from lesions of the posterior thalamus.19, 2o In the previously described patient, the clinical findings were u n u s u a l l y subtle, w i t h no d o c u m e n t a b l e neurologic findings of speech d i s t u r b a n c e or m e m o r y i m p a i r m e n t . N o r w a s there any evidence of sensory, motor, or cranial nerve dysfunction despite independent examination by two emergency physicians. This patient could have been dismissed as having a hyperventilation syndrome and a c u t e a n x i e t y given h e r absence of neurologic findings and a docum e n t e d respiratory alkalosis w i t h o u t hypoxia. H o w e v e r , h y p e r v e n t i l a t i o n was an u n l i k e l y diagnosis because of the u n i l a t e r a l nature of her paresthesias w i t h sparing of the perioral region, a b s e n c e of carpopedal spasm, and lack of psychiatric history. Annals of Emergency Medicine
SUMMARY T h e case of a 52-year-old diabetic and h y p e r t e n s i v e w o m a n w h o presented w i t h c o m p l a i n t s of right sided p a r e s t h e s i a s is r e p o r t e d . She w a s f o u n d to h a v e a t h a l a m i c h e m o r rhage. This case, as well as the brief r e v i e w of p r e v i o u s c l i n i c a l reports, should alert the e m e r g e n c y p h y s i c i a n to consider the possibility of t h a l a m i c insult in any p a t i e n t comp l a i n i n g of hemiparesthesias, particularly older patients w i t h a h i s t o r y of h y p e r t e n s i v e disease. T h e diagnosis should also be considered in patients w i t h speech or m e m o r y i m p a i r m e n t or h e m i - i n a t t e n t i o n s y n d r o m e s , regardless of w h e t h e r clinical evidence of sensory or m o t o r deficit is present.
REFERENCES
1. Piepgras U, Rieger P: Thalamic bleeding: Diagnosis, course, and prognosis. Neuroradiology 1981;22:85-91. 2. Fisher CM: The pathological and clinical aspects of thalamic hemorrhage. Trans A m Neurol Assoc 1959;84:56-59. 3. Barracquer-BordasL, Illa I, Escartin A, et al: Thalamic hemorrhage: A study of 23 patients with diagnosis by computerized tomography. Stroke 1981;12:524-527. 4. Weisberg L: Thalamic hemorrhage: ClinicalCT correlations. Neurology 1986~36:1382q386. 5. Fazio C, Sacco G, Bugiani O, et al: The thalamic hemorrhage: An anatamo-clinical study. Eur Neurol 1973;9:30-43. 6. Goto N, Kaneko M, Muraki M, et al: Thalamic hemorrhage - A clinicoanatomic study. Neurol Med Chir (Tokyo) 1982;22:24-36. 7. Hankey G, Stewart-Wynne E: Anmesia following thalamic hemorrhage. Stroke 1988;19: 776-778. 8. Kawahara N, Sato K, Muraki M, et al: CT classification of thalamic hemorrhages and their clinical implications. Neurology 1986;36: 165-172. 9. Choi D, Sudarsky L~Schacter S, et al: Medial thalamic hemorrhage with amnesia. Arch Neurol 1983~40:611-613. 10. Waxman S, Ricaurte G, Tucker S, et al: Thalamic hemorrhage with neglect and memory disorder. ] Neurol Sci 1986;75:105-112. ll, Santamaria J, BlesaR, Tolosa E, et ah Confnsional syndrome in thalamic stroke. Neurology 1984;34:1618. 12. Maiuri F, Signorella C, Collela G, et al: Aphasia and left thalamic hemorrhage. Clin Neurol Chir 1983~1:20-24. 13. Leiguarda R: Environmental reduplication associated with a right thalamic hemorrhage. [ Neurol Neurosurg Psychiatry 1983;46:1154. 14. Kosten T, Rappaport A: Left thalamic hemorrhage and aphasia. Corm Med 1982;4:633-635. 15. Kirshner H, Kistler K: Aphasia after right thalamic hemorrhage. A r c h N e u r o l 1982 i 39:667-669. 19:7 July 1990
16. C h e s s o n A: A p h a s i a following a right thalamic hemorrhage. Brain Language 1983;19: 306-316.
18. Verma A, Maheshwari M: Hypestheticataxic-hemiparesis in thalamic hemorrhage. Stroke 1986;7:49-51.
17. Ciemens V: Localized thalamic hemorrhage. Neurology 1970;20:776-782.
19. Hirose G, Kosoegawa H, Saeki M, et al: The syndrome of posterior thalamic hemorrhage.
19:7 July 1990
Annals of Emergency Medicine
Neurology 1985;35:998-1002. 20. Hier D, Davis K, Richardson g Jr, et al: Hypertensive putaminal hemorrhage. Ann Neurol 1977;1:152-159.
819/133