Amyloid angiopathy is the most common cause of spontaneous non-hypertensive hemorrhage in elderly patients, and is usually lobar in location (as in the case). They often appear in association with Alzheimer's disease (CTO Manual). The response that may cause the most doubts is 2, hypertension, but the most frequent localizations are: putamen, thalamus, pons and cerebellum. Therefore, most of the time these are deep hemorrhages (CTO Manual). In addition, as a clue it tells us that the patient has well-controlled hypertension without drugs, although this data would not serve to rule out the response. Answer 1, a malformation is typical of young patients, rare in older people. It also decreases the chance of not finding a malformation with contrast-enhanced CT. Answer 4, a brain tumor, does not seem likely since the mass is not seen on CT, and as in the previous case, it is more difficult not to find such a lesion after contrast administration. Answer 3 does not seem correct since vasculitis is a rare entity and more so in older people.

Amyloid angiopathy is the most common cause of spontaneous non-hypertensive hemorrhage in elderly patients, and is usually lobar in location (as in the case). They often appear in association with Alzheimer's disease (CTO Manual). The response that may cause the most doubts is 2, hypertension, but [HIDDEN] are: putamen, thalamus, pons and cerebellum. Therefore, most of the time these are deep hemorrhages (CTO Manual). In addition, as a clue it tells us that the patient has well-controlled hypertension without drugs, although this data would not serve to [HIDDEN]. Answer 1, a malformation is typical of young patients, rare in older people. It also decreases the chance of not finding a malformation with contrast-enhanced CT. Answer 4, a brain tumor, does not seem likely since [HIDDEN], and as in the previous case, it is more difficult not to find such a lesion after contrast administration. Answer 3 does not seem [HIDDEN] since vasculitis is a rare entity and more so in older people.

An 80-year-old man is admitted for a sudden onset of aphasia and right hemiparesis. His history includes hypertension, well controlled with diet and cognitive deterioration in the last year under study by his neurologist. The emergency cranial CT scan shows a left frontal lobar hematoma without contrast uptake. What is the most probable cause of the hematoma?

Arteriovenous malformation masked by acute hematoma.

Isolated vasculitis of the nervous system.

Cerebral amyloid angiopathy (congophilic angiopathy).

[A case report of simultaneous multiple intracerebral hematomas].

A case of multiple spontaneous intracerebral hematomas is presented. A 67-year-old man with 7 years history of hypertension had sudden clumsiness in his right hand and an hour later dysarthria appeared. A CT scan taken 3 hours after the onset revealed two well demarcated high density areas in the left putamen and in the parietal subcortex. A diagnosis of multiple intracerebral hematomas was made. On neurological examination he was midly stuporous (13 points of Glasgow Coma Scale). Dysarthria, right hemiparesis and right extensor plantar response were seen. CT scan of 6 hours later disclosed the same findings as the previous study. He recovered well and neurologically free in a few days. On the following CT scans both hematomas were isodense 2 weeks later, and ring-like enhancement effect was noted. CT scan showed normal appearance 7 weeks later. On MRI using 0.5 T unit t-1 and t-2 weighted spin echo images of these hematomas also showed the similar chronological changes. The history, these CT and MRI studies suggest that two hematomas of this case occurred almost simultaneously in one cerebral hemisphere. No causative factors such as blood dyscrasias, AVM, angioma, septicemia, malignancies or sinus thrombosis was identified. We consider that a hypertensive intracerebral hematoma of the putamen was followed by the parietal intracerebral hematoma within a few hours, although amyloid angiopathy was not completely excluded because no cerebral biopsy of the lesion was performed.

[Cerebral amyloid angiopathy complicated by multiple cerebral infarcts and intracerebral hemorrhages: case report].

Recently, cerebral amyloid angiopathy is stressed as an unusual and infrequent cause of cerebral infarct or intracerebral hemorrhage. This report described a case of cerebral amyloid angiopathy complicated by multiple cerebral infarcts and multiple intracerebral hemorrhages. This 70-year-old man was admitted to our hospital on November 10, 1984 for evaluation of the gradual onset of dysarthria. Examination showed only slight dysarthria. There was no history of hypertension or dementia. A computed tomography (CT) showed enlarged ventricles with cortical atrophy and multiple low-density lesions, deep in the left frontal, left parietal, right parietal lobes, and in the both basal ganglias. The patient discharged from the hospital with only slight dysarthria. On November 20, 1984, he was admitted to our hospital again, because he was found unresponsive on the floor. He was somnolent but arousable. Examination showed disorientation, impairment of recent memory and impairment of calculation, A CT scan demonstrated three small intracerebral hemorrhages in the left frontal, right parietal lobes and left basal ganglia. On the fifth hospital day he deteriorated acutely, becoming semicomatose and hemiparetic on the right side. A repeated CT scan showed two new intracerebral hemorrhages in the left frontal lobe. Cerebral angiograms showed only minimal changes due to the occupying lesions in the above mentioned area. The hematomas was evacuated via left fronto-parietal craniotomy. The specimens removed with hematoma (stained with hematoxylin-eosin, Congo red and thioflavin T) showed extensive amyloid angiopathy. Postoperatively he made a good recovery, although he had residual mental dysfunctions. He expired by pneumonia on March 30, 1985.(ABSTRACT TRUNCATED AT 250 WORDS)

A restricted subarachnoid hemorrhage in the cortical sulcus in cerebral amyloid angiopathy: could it be a warning sign?

Cerebral amyloid angiopathy is a well-known disease that is predominantly recognized in elderly people and repeatedly causes large subcortical hemorrhages. These hemorrhages may be derived from vessel wall weakness because of Abeta depositions in the wall of the cortical and leptomeningeal arteries. Although vessel ruptures in CAA have been thought to occur in cortical arteries, it was recently demonstrated that the primary hemorrhage occurs in the subarachnoid space, particularly the cerebral sulci, as a result of multiple ruptures of meningeal arteries in some cases of subcortical hematoma caused by CAA. Case patient 1 was a 74-year-old woman who presented with epileptic seizure. A restricted SAH in the right frontal lobe was observed on MRI. Thirty-three days later, left hemiparesis occurred suddenly and a huge subcortical hematoma was observed in the right frontal lobe on CT. The hematoma was removed, and the patient was pathologically diagnosed with amyloid angiopathy. Case patient 2 was a 73-year-old man who presented with epileptic seizure. A restricted SAH in the right frontal lobe was observed on MRI. Twenty days later, left hemiparesis occurred suddenly and a huge subcortical hematoma was observed in the right frontoparietal area on CT. Hematoma removal was performed on both patients, and they were diagnosed pathologically with amyloid angiopathy. We report on the cases of 2 patients with CAA who presented with epileptic seizure and were found to have a restricted subarachnoid hematoma in the cerebral sulcus on MRI before their subcortical hemorrhages occurred. Both cases were diagnosed pathologically. This demonstrated that vessel ruptures in CAA can occur in the subarachnoid space, particularly the cerebral sulci, as a result of ruptures of meningeal arteries. A restricted SAH on CT/MRI could be a warning sign of a huge subcortical hemorrhage in CAA.

Lobar intracerebral hemorrhage. A clinical, radiographic, and pathological study of 29 consecutive operated cases with negative angiography.

The authors operated consecutively on 50 patients with lobar intracerebral hemorrhage during a prospectively designed study period from January, 1986, to March, 1990. They investigated the correlations between the underlying causes and the clinicoradiographic features in 29 patients who showed no angiographic vascular abnormalities, in order to elucidate the operative indication for such cases. Patients with ruptured saccular aneurysm or trauma were not included in this study. There were 15 males and 14 females, ranging in age from 7 to 76 years (mean 52.4 years). Histological diagnoses of the surgical specimens were as follows: vascular malformation in nine cases (arteriovenous malformation (AVM) in six and cavernous malformation in three), microaneurysm in 11, cerebral amyloid angiopathy in six, and brain tumor in two; in the remaining case the cause was not verified histologically. The underlying cause was determined in 96.5% of cases. The mean patient age was lowest in the cavernous malformation group (27.0 years), followed by the AVM (45.8 years), microaneurysm (59.8 years), and cerebral amyloid angiopathy (70.0 years) groups. Four patients with vascular malformation (three AVM's and one cavernous malformation) had previous episodes of bleeding at the same site, whereas none of those with microaneurysms or cerebral amyloid angiopathy had such episodes. On computerized tomography (CT) scans, the round to oval hematoma was related to the presence of an AVM or cavernous malformation in contrast to microaneurysms and cerebral amyloid angiopathy. Upon infusion of contrast material, variable enhancement was seen in five (two AVM's and three cavernous malformations) of the nine vascular malformations while no enhancement was noted in any patient with microaneurysm or cerebral amyloid angiopathy at the acute stage. Subarachnoid extension of the hematoma was associated with cerebral amyloid angiopathy significantly more frequently than with AVM's (p less than 0.05) and microaneurysms (p less than 0.01). The results suggest that clinicoradiographic pictures in cases with negative angiography are quite different among the three major pathological categories; namely, vascular malformation (AVM and cavernous malformation), microaneurysm, and cerebral amyloid angiopathy. It is suggested that the underlying etiology of a given lobar intracerebral hemorrhage with negative angiography may be predicted by a combination of patient age, history of previous bleeding at the same site, hematoma shape, and subarachnoid extension of the hematoma on CT scans. Based upon these findings, the authors discuss operative indications for such cases.

[A case of primary subarachnoid hemorrhage due to cerebral amyloid angiopathy].

A 77-year-old man who was suffering from an intracerebral hemorrhage of the left subcortex without hypertension was admitted to our hospital. The only neurological symptom was right arm monoparesis. Brain MRI demonstrated a subarachnoid hemorrhage (SAH) in the left frontal lobe. On the day of admission, conventional cerebral angiography revealed no abnormalities in brain arteries. His symptom was disappeared immediately after admission. He was discharged without neurological deficit on day 25. However, he was rehospitalized in our hospital on the same day because he experienced a right subcortical hemorrhage. The neurological symptoms were consciousness disturbance, aphasia and right hemiparesis. Brain CT disclosed a subcortical hemorrhage in the left temporal lobe. CT stereo-guided drainage was performed. Then, we examined tissue removed from the brain's surface. Histologically, beta-amyloid protein was deposited on the walls of the meningeal and cortical vessels, and it replaced all the layers of those walls. Therefore, a diagnosis of cerebral amyloid angiopathy (CAA) was made. His condition gradually improved, but CT showed an asymptomatic ICH in the right parietal lobe on day 36. On day 47, he had a symptomatic ICH in the left caudate nuclei and right frontal lobe. He died on day 66 because of pneumonia. Intracranial hemorrhages due to CAA have been reported and the majority of the lesions have been lober hemorrhage. To the best of our knowledge, few reports have been published regarding primary SAH caused by CAA. The cause of SAH should be considered as CAA when SAH appears without hypertension or in elderly patients.

[Case report of a "probable" cerebral amyloid angiopathy].

Sixty-two year old man was admitted to the department of neurosurgery after stroke episode. CT-scan revealed non-traumatic, non-hypertensive intracerebral hemorrhage in the left temporal lobe; cerebral amyloid angiopathy was suspected. Initially, according to Boston criteria, intracerebral hematoma was interpreted as a result of a "probable" cerebral amyloid angiopathy. Surgical evacuation of the hematoma lead to the partial recourse of speech and cognitive deficit. Four weeks after stroke onset and 3 weeks after surgery CT was performed, which revealed intracerebral hematoma in the right parietal lobe; this fact let to diagnose "probable" cerebral amyloid angiopathy. The second hematoma was evacuated, and surgical treatment together with medical therapy improved patient's quality of life. Treatment strategy for the intracerebral hematomas resulting from cerebral amyloid angiopathy has not been justified yet, which requires further investigations.

Repeated recurrent intracerebral hemorrhage may be involved in cerebral amyloid angiopathy-related inflammation: An autopsy case.

We report an autopsy case of repeated recurrent intracerebral hemorrhage (ICH) diagnosed as having cerebral amyloid angiopathy-related inflammation (CAA-ri) in a 65-year-old woman. She had no history of hypertension or other risk factors for stroke. She had a history of lobar ICH in the right parietal lobe 30 months prior. Follow-up magnetic resonance imaging (MRI) performed 29 months after the initial ICH revealed superficial siderosis in the left frontal lobe. She initially presented with severe headache and dysarthria. An initial computed tomography (CT) revealed a subarachnoid hemorrhage on the left frontal lobe. One hour later, an epileptic seizure occurred, and another CT performed at the time revealed lobar ICH in the frontal lobe. Emergency surgical hematoma evacuation was performed. The cortical artery was removed from the surgical specimen. Hematoxylin and eosin (HE) staining revealed lymphocytic perivascular cuffs, and immunohistochemical staining revealed abundant amyloid-β (Aβ) deposits. The patient was diagnosed as having CAA-ri. On the next day, and 19, 46, 55, 78, 79, and 85 days after admission, ICH recurred. We did not administer immunosuppressive drugs, such as high-dose corticosteroids or cyclophosphamide, because of the patient's condition. Following the last ICH, the patient died on the 90th day after symptom onset. An autopsy was performed. Histologically, abundant Aβ deposits were observed within the leptomeningeal and cortical arteries. Further dense-cored amyloid plaques were observed in the cortical samples. Our findings that ICH occurred initially three times in the left hemispheres and later five times in the right hemispheres were considered immune-mediated effects on vascular function. Further, superficial hemosiderosis in the left frontal lobe occurred before the first three ICH events, and hyperintensity of the white matter on MRI was identified in the right parietal lobe, a typical finding of CAA-ri. We hypothesize that the inflammatory process in CAA-ri may be related to recurrent ICH.

Inflammatory cerebral amyloid angiopathy: the overlap of perivascular (PAN-like) with vasculitic (Aβ-related angiitis) form: an autopsy case.

Beside advanced age, cerebral amyloid angiopathy (CAA) and hypertension (HTA) are the two most important risk factors for haemorrhagic stroke. Inflammatory changes of amyloid-laden vessels have been reported only in rare sporadic CAA cases. We present the case of a 78-year-old woman with a history of hypertension, dementia and haemorrhagic stroke of the right frontal lobe 2 years before admission. She was admitted with recurrence of symptoms of transient aphasia and central, right-side facial paresis that occurred an hour before her arrival at the hospital. In the admission unit, she was only slightly confused, with no other neurological deficits. An urgent CT scan revealed a recent haemorrhagic stroke in the left frontal lobe. In an hour her condition suddenly deteriorated. After a generalized seizure she presented with right-side hemiparesis with signs of uncal herniation and remained unconscious. A control CT scan showed a large haemorrhagic expansion that comprised the whole left brain hemisphere with 2 cm midline shift. She died about 10 hours after the onset of symptoms. At autopsy chronic inflammation of the thyroid gland, bronchopneumonia, fibrous and fatty heart degeneration and kidney haemorrhagic infarcts were documented. Amyloid deposition and systemic immune disorders in the inner organs were not demonstrated. In neuropathological examination we diagnosed inflammatory form of CAA with coexistence (the overlap) of two, perivascular and vascular, subtypes of CAA-related inflammation.

[Four cases of cerebral venous angioma--with special reference to its surgical indication and CT diagnosis].

Four cases of venous angioma, one cerebral and three in the cerebellum, are reported. Case 1. A 50-year-old woman who had a sudden attack of headache and disorientation was admitted to the Mitsui Memorial Hospital. Neurological examination revealed slight disorientation, mild motor aphasis and right hemiparesis. Plain CT scan on admission showed a left frontal hematoma. Left cerebral angiomas demonstrated a caput-Medusae-like lesion which consisted of numerous small veins and drained into one single enlarged vein. Enhanced CT scan taken 12 days after the attack demonstrated a linear enhancement next ot the hematoma. Left frontal craniotomy was performed, and the hematoma was evacuated. In the next step, coagulation and resection of the major part of the angioma was attempted. However, this caused significant swelling of the adjacent brain and the angioma had to be resected totally including intervening normal cerebral tissue. Postoperatively, the patient became worse with significant hemiparesis and severe motor aphasia. After intensive rehabilitation treatment, she recovered gradually and was discharged on foot with moderate speech disturbances. Histological examination revealed a typical venous angioma with hyalinization of vessel wall. Case 2. A 55-year-old woman with a 9 year history of vertigo and headache was admitted to our hospital because of sudden onset of numbness in her right lower limb. Enhanced CT scan revealed a small nodular high density lesion and an old hematoma in the right cerebellar hemisphere. Vertebral angiograms demonstrated a single abnormal vein with some small veins in the right cerebellum. Right suboccipital craniectomy was performed and the blood clot was removed. The abnormal veins were electro-coagulated. The postoperative course was uneventful and the patient was discharged with no neurological deficit. Case 3. A 31-year-old man was admitted to our department with 9 month history of nausea and vertigo attack. Enhanced CT scan demonstrated a large nodular high density lesion in the left cerebellar hemisphere. Vertebral angiograms showed a typical caput-Medusae-like venous angioma. The patient had no evidence of hemorrhage and was discharged without surgery. Case 4. A 36-year-old man who had two attacks of nausea and headache was admitted to the Mitsui Memorial Hospital. Enhanced CT scan showed a linear high density lesion in the right cerebellar hemisphere. Vertebral angiograms disclosed a typical venous angioma in the right cerebellum. This patient also had no attack of bleeding and was discharged without operation.(ABSTRACT TRUNCATED AT 250 WORDS)

[Three cases of cryptic arteriovenous malformation in basal ganglia manifested by putaminal hemorrhage].

Three cases of histologically proven cryptic arteriovenous (AV) malformation of the basal ganglia are reported. Seventeen cases of patients showing putaminal hemorrhage in the CT scan underwent craniotomy for evacuation of a hematoma between January 1986 and December 1988. The preoperative diagnosis was hypertensive putaminal hemorrhage. In all three cases a network of abnormal vessels around the internal capsule was detected at surgery. Case 1: A 62-year-old male was admitted to our hospital with consciousness disturbance (JCS 20), total aphasia and right hemiparesis. The CT scan showed left putaminal hemorrhage. The volume of the hematoma was 45 ml by CT criteria. Left carotid angiography did not demonstrate any abnormal findings. Case 2: 69-year-old male was admitted with consciousness disturbance (JCS 10) and right hemiparesis. Left putaminal hemorrhage (volume 25 ml) was recognized on the CT scan. Two hours after admission, the consciousness level suddenly deteriorated (JCS 100). At that moment, the volume of the putaminal hematoma had increased to 100 ml. AV malformation was not detected by left carotid angiography. Case 3: A 50-year-old male was admitted with consciousness disturbance (JCS 20), total aphasia and right hemiparesis. The CT scan showed left putaminal hemorrhage of 73 ml. Pathohistological examination proved AV malformation in each case. The three cases described here suggest the following; 1) The incidence of the basal ganglia cryptic AV malformation has been considered low, but meticulous examination shows that among the cases diagnosed as hypertensive hemorrhage, AV malformation is not infrequently the hidden cause.(ABSTRACT TRUNCATED AT 250 WORDS)

[Lobar intracerebral hemorrhage secondary to cerebral amyloid angiopathy: a clinicopathologic study of three operated cases].

Three operated cases of lobar intracerebral hemorrhage (LICH) related to cerebral amyloid angiopathy (CAA) were studied clinicopathologically. They constituted about 8% of all LICH cases (n = 37) operated upon in our institute (DUSM) during the past 3 years. Case 1, 2 and 3 aged 71, 67 and 73 years, respectively. There were 2 males (Cases 1 & 2) and 1 female (Case 3). Only one case (Case 3) had both hypertension and dementia before hemorrhage. In all 3 cases, neurologic symptoms deteriorated after admission. The hematoma involved the right temporo-parietal in 1 (Case 1), the right parieto-occipital in 1 (Case 2) and the left fronto-parietal region in 1 (Case 3). Case 1 developed a new hematoma in the right occipital lobe on the day following surgery. On CT, the hematoma was multilobular in shape and located very superficially extending to the subarachnoid space in all cases. There was no abnormal enhancement in and around the hematoma upon contrast infusion. Angiography showed only an avascular mass sign in case. At surgery, the hematoma was extruded onto the cortical surface in all cases. The surgical outcome was good in 2 (Cases 1 & 2) and fair in 1 (Case 3). Removed hematomas, solid nodular tissues and adjacent brain tissues were examined histologically using hematoxylin and eosin, Azan-Mallory, elastica van Gieson, silver and Congo red stains. Arteries in the hematoma wall, the subarachnoid space and the adjacent brain parenchyma were intensely stained with Congo red and showed birefringence on polarized light.(ABSTRACT TRUNCATED AT 250 WORDS)

[Two cases of elderly patients with ruptured AVM with contrast medium extravasation during cerebral angiography].

Two cases are reported of elderly patients who experienced intracranial extravasation of contrast medium (CM) during carotid angiography (CAG) for ruptured cerebral arteriovenous malformations (AVM). The first patient, an 87-year-old male with no history of hypertension, was admitted immediately following a loss of consciousness after swimming in a pool. CT scan revealed a large intracranial hematoma in the left frontal lobe. CAG performed 1 hour after his arrival revealed a small AVM, fed by the left anterior cerebral artery with concomitant extravasation of CM. The patient's condition subsequently deteriorated and he died the following day. The second patient, a 71-year-old female, was admitted to our hospital in a comatose state after complaining of a severe headache. CT scan revealed a right parietal lobe hemorrhage extending into the ventricles. CAG was performed and demonstrated a small AVM in the right parietal lobe with extravasation of CM. Following emergency removal of the hematoma and AVM, the patient regained consciousness although some motor deficits persisted. A literature review revealed that only 6 cases of CM extravasation with ruptured AVM have been previously reported. The 4 previous cases involved patients 9, 15, 33 and 66-year-old, the younger three of which had a good outcome. The patients reported here were much older, and had a much less favorable outcome. Thus, AVM with CM extravasation may have a better prognosis in younger individuals.

[A case favorably progressed after operation for hypertensive intracerebral hemorrhage showed extravasation on angiogram occurred in chronic alcoholism].

It is said that the prognosis is generally unfavorable in patients with hypertensive intracerebral hemorrhage showed extravasation on angiogram. Recently, we experienced a case whose prognosis was eventful after the removal of hematoma. So we reported this case and discussed between alcoholism and intracerebral hemorrhage accompanied with extravasation on angiogram in this paper. A 59-year-old male was transferred to our emergency center because of right hemiplegia and mild clouding of consciousness at around nine in the evening on December 12, 1983. At the time of admission, his neurological state was classified into grade II, exhibiting the right putamenal hemorrhage and pyramidal destruction type of hematoma by CT scan with 58 ml of hematoma volume. The right carotid angiography was immediately performed and confirmed the hematoma being of lateral type. At that time, extravasation proximal to the lateral lenticulostriate artery was noted. Repeated CT scan revealed the enlarged hematoma (105 ml) accompanying with ventricular hemorrhage. At the completion of these examinations, the neurological grade was III. The hematoma was surgically removed after 4 hours following the onset of cerebral hemorrhage. His postoperative course was very favorable. Although acute hydrocephalus appeared later on, it was cured by ventricular drainage. The patient become possible to walk with a helper by 1 month after operation. CT scan obtained 1 month after operation revealed a remarkable brain atrophy, which was probably derived from chronic alcoholism.(ABSTRACT TRUNCATED AT 250 WORDS)

[A case of hypertensive intracerebral hemorrhage associated with cerebral arteriovenous malformation and aneurysm (author's transl)].

A 45-year-old man suddenly developed right hemiparesis and aphasia during work and lost conciousness next day, when he was admitted to us. Lumbar puncture showed bloody C.S.F. with the initial pressure of 220 mm H2O. Physical examination revealed hypertension and arteriosclerosis. Cerebral angiogram revealed an arteriovenous malformation in the left frontoparietal-parasagittal region and a saccular aneurysm at the left internal carotid-posterior communicating artery junction. In addition, the existence of putaminal hematoma was suspected on account of the displacement of the left anterior cerebral artery and the left lenticulostriate arteries. On the fourth day after admission his consciousness returned and the right hemiparesis gradually improved. One month later the disappearance of the displacement of the anterior cerebral artery was demonstrated by cerebral angiogram. A frontoparietal craniotomy was done and no hematoma was found around the arteriovenous malformation and the basis of the aneurysm did not adhere to the temporal lobe. Taking these findings into consideration, it is presumed that the hematoma in putaminal region was due to neither arteriovenous malformation nor aneurysm but was a hypertensive intracerebral hemorrhage.

List of MeSH codes (C14)

– intracranial arterial diseases – cerebral arterial diseases – cadasil – cerebral amyloid angiopathy – cerebral amyloid angiopathy, familial – infarction, anterior cerebral artery – infarction, middle cerebral artery – infarction, posterior cerebral artery – intracranial aneurysm – intracranial arteriosclerosis – dementia, vascular – intracranial arteriovenous malformations – intracranial hemorrhages – cerebral hemorrhage – basal ganglia hemorrhage – putaminal hemorrhage – cerebral hemorrhage, traumatic – intracranial hemorrhage, hypertensive – intracranial hemorrhage, traumatic – brain hemorrhage, traumatic – brain stem hemorrhage, traumatic – cerebral hemorrhage, traumatic – hematoma, epidural, cranial – hematoma, subdural – hematoma, subdural, acute – hematoma, subdural, chronic – hematoma, subdural, intracranial – subarachnoid hemorrhage, traumatic – pituitary apoplexy – subarachnoid hemorrhage

Density heterogeneity and fluid-blood levels in patients aged over 55 with lobar hematoma.

Density heterogeneity and fluid-blood levels (FBLs) are frequently seen on acute CT scans of deep brain hemorrhage. Our aim was to analyze the density heterogeneity and FBLs seen on acute/subacute CT in patients aged>55 with lobar haemorrhage (LH), and to study the relationship of these brain abnormalities with other parameters, including cerebral amyloid angiopathy (CAA)-related abnormalities. This was an observational study and retrospective analysis of early CT scans (<7 days) in patients aged>55 years with acute lobar hemorrhage who, between 2012 and 2015, were entered into our stroke database. A total of 37 LH episodes (without trauma, abnormal coagulation/platelet counts, vascular malformation, tumor or vasculitis) in 35 patients were analyzed. Other studied parameters were gender, age, history of hypertension, blood pressure on admission, prior antiplatelet treatment, aPTT, PTT, platelet count, hematocrit, timing of first CT, LH volume, involved lobe, cortical superficial siderosis, microbleeds, chronic LH and CAA (classic and modified Boston) criteria. CAA-related abnormalities seen on MRI were also scored. Overall, in 26 LH episodes (70%), CT was performed within 24h. Density heterogeneity and FBLs were seen in 19 (51%) and 9 (24%) LH episodes, respectively. Also, according to classic and modified Boston criteria, 18 (51%) and 24 (69%) patients, respectively, fulfilled criteria for probable/definite CAA. As for the presence of FBLs, a statistically significant association was found with both the presence of probable/definite CAA according to modified Boston criteria (P=0.033) and the presence of superficial siderosis (P=0.019). Density heterogeneity and, to a lesser degree, FBLs are frequently seen in patients aged>55 with LH. FBLs may also be associated with CAA-related hemorrhage.

Mixed cerebrovascular disease in an elderly patient with mixed vascular risk factors: a case report.

Mixed cerebrovascular disease is a diagnostic entity that presents with hemorrhagic and ischemic stroke clinically and/or subclinically. Here, we report a patient with mixed vascular risk factors, who presented with multiple intracerebral hemorrhages and a simultaneously occurring cerebral infarction with hemorrhagic transformation. A 63-year-old male with no history of trauma or prior neurological disease presented with a sudden onset of weakness in his right limbs, followed by an episode of focal seizure without impaired awareness. The patient had a 4-year history of deep vein thrombosis in the lower limbs, and a 2-year history of Raynaud's phenomenon in the hands. He also had a family history of hypertension and thrombophilia. Head computed tomography plain scans showed two high densities in the bilateral parietal lobes and one mixed density in the left frontal lobe. The patient was diagnosed with mixed cerebrovascular disease. In this report, we make a systematic clinical reasoning regarding the etiological diagnosis, and discuss the possible pathogenic mechanisms leading to mixed cerebrovascular disease. We exclude coagulopathy, endocarditis, atrial fibrillation, patent foramen ovale, brain tumor, cerebral venous thrombosis, cerebral vascular malformation, cerebral amyloid angiopathy and vasculitis as causative factors. We identify hypertension, hereditary protein S deficiency, hypercholesteremia and hyperhomocysteinemia as contributing etiologies in this case. This case presents complex underlying mechanisms of mixed cerebrovascular disease, in which hypertension and hyperhomocysteinemia are considered to play a central role.

First_Aid_Step2

(A) CT scan without contrast reveals blood in the subarachnoid space at the base of the brain (arrows). (B) A normal CT scan without contrast shows no density in this region (arrows). (Reproduced, with permission, from Aminoff MJ. Clinical Neurology, 3rd ed. Stamford, CT: Appleton & Lange, 1996: 78.) ■ Surgical clipping is the defnitive treatment for aneurysms. Endovascular coiling is an option for poor surgical candidates. Risk factors include hypertension, tumor, amyloid angiopathy (in the elderly), anticoagulation, and vascular malformations (AVMs, cavernous hemangiomas). Hx/PE: Presents with focal motor and sensory defcits that often worsen as the hematoma expands. Severe headache of sudden onset, nausea/ vomiting, seizures, lethargy, or obtundation may also be seen. Dx: Immediate noncontrast head CT (see Figure 2.10-5). Look for mass effect or edema that may predict herniation.

List of MeSH codes (C10)

– hematoma, epidural, cranial – hematoma, subdural – hematoma, subdural, acute – hematoma, subdural, chronic – hematoma, subdural, intracranial – subarachnoid hemorrhage, traumatic – pituitary apoplexy – subarachnoid hemorrhage – subarachnoid hemorrhage, traumatic – leukomalacia, periventricular – sneddon syndrome – vascular headaches – vasculitis, central nervous system – aids arteritis, central nervous system – lupus vasculitis, central nervous system – temporal arteritis – vasospasm, intracranial – vertebral artery dissection – dementia – aids dementia complex – alzheimer disease – primary progressive aphasia – creutzfeldt-jakob syndrome – dementia, vascular – dementia, multi-infarct – huntington disease – Klüver-Bucy syndrome – lewy body disease – pick disease of the brain – diffuse cerebral sclerosis of schilder – encephalitis – encephalomyelitis – limbic encephalitis – meningoencephalitis

[A case of multiple cerebral hemorrhage related to cerebral amyloid angiopathy].

A case of multiple cerebral hemorrhage in the bilateral parietal lobes related to cerebral amyloid angiopathy (CAA) is reported. A 66-year-old man was admitted to our hospital because of headache and vomiting on Feb. 21, 1983. He had no history of hypertension, diabetes mellitus, recent head injury, or dementia. Four days prior to admission, he had behaved as if he were blind, but, had denied any blindness. On examination, he was confused and disoriented. Blood pressure was 130/80 mmHg. Abnormal findings on neurological examination included memory disturbance, apraxia for dressing, right-left disorientation, finger agnosia and Balint's syndrome. A CT scan showed multiple subcortical hematomas in the bilateral parietal lobes. Intracerebral hemorrhage related to CAA was suspected. Confirmation of the presence of amyloid in the cerebral vessels was established by examination of brain biopsy specimens. The characteristics of cerebral hemorrhage related to CAA are as follow--occurrence in elderly, sometimes demented people; localization to the cortex and subcortical white matter, with direct extension into the subarachnoid space; frequent multiple occurrence in time and/or at several sites within the cerebral hemispheres; sometimes occurrence after operative procedures or head injuries. A specific diagnosis of CAA can only be made by histological examination, but the indication of brain biopsy should be carefully decided because of hemostatic difficulty and tendency to rebleed. In conclusion, CAA should be considered as a cause of hemorrhage in elderly patients who are often normotensive and demented.

[Spontaneous intracerebral hematomas: occipital lobe hemorrhages].

Spontaneous intracerebral hematomas can be diagnosed immediately and localized exactly by the means of cranial computerized tomography. The occipital lobe is a relatively rare site of hypertensive hematomas which are the most frequent etiologic group. Out of 264 patients with intracerebral hematomas ion cranial computerized tomography we found the occipital lobes affected in 24 cases i.e. 9%. 116 patients with intracerebral hematomas treated in the neurologic clinic demonstrated in 15 cases (13%) occipital localization. In 7 patients bleedings were of hypertensive origin, in 4 cases etiology was unknown, in one case it originated from an arteriovenous angioma and in 3 cases congophilic (amyloid) angiopathy was the basic disease. In smaller occipital hematomas the clinical symptoms are relatively mild, mainly consisting of acute headache and hemianopsia. If the hematoma is limited to the occipital lobe the prognosis is favorable both with or without neurosurgical treatment.

First_Aid_Step1

Crescent-shaped hemorrhage (red arrows in C and D ) that crosses suture lines. Can cause midline shift (yellow arrow in C ), findings of “acute on chronic” hemorrhage (blue arrows in D ). EF due to trauma, or rupture of an aneurysm (such as a saccular aneurysm E ) or arteriovenous malformation. Rapid time course. Patients complain of “worst headache of my life.” Bloody or yellow (xanthochromic) lumbar puncture. Vasospasm can occur due to blood breakdown  ischemic infarct; nimodipine used to prevent/reduce vasospasm.  risk of developing communicating and/or obstructive hydrocephalus. Most commonly caused by systemic hypertension. Also seen with amyloid angiopathy (recurrent lobar hemorrhagic stroke in elderly), vasculitis, neoplasm. May be 2º to reperfusion injury in ischemic stroke. Hypertensive hemorrhages (Charcot-Bouchard microaneurysm) most often occur in putamen of basal ganglia (lenticulostriate vessels G ), followed by thalamus, pons, and cerebellum H .

Cerebral amyloid angiopathy

Diagnosis CAA can only be definitively diagnosed by a post-mortem autopsy. Biopsies can play a role in diagnosing probable cases. When no tissue is available for biopsy, the Boston Criteria are used to determine probable CAA cases from MRI or CT scan data. The Boston Criteria require evidence of multiple lobar or cortical hemorrhages to label a patient as probably having CAA. Susceptibility weighted imaging has been proposed as a tool for identifying CAA-related microhemorrhages. Imaging Cerebral amyloid angiopathy can be presented with lobar intracerebral hemorrhage or microbleeds in the brain. The bleeding usually occurs on the surfaces of the brain in contrast with intracranial haemorrhage due to high blood pressure which occurs deep locations of the brain such as basal ganglia and pons. In lobar intracerebral bleed, computed tomography (CT) scan would show hyperdense haemorrhage area and hypodense odema around the haemorrhagic site.

[A case of cerebral amyloid angiopathy in which a restricted subarachnoid hemorrhage recurred in the cortical sulcus following a subcortical hemorrhage].

Cerebral amyloid angiopathy (CAA) is predominantly recognized in elderly people and repeatedly causes a huge subcortical hemorrhage. Some cases of CAA can cause secondary subarachnoid hemorrhage (SAH), but cases in which it causes primary SAH is very rare. We describe a valuable reference case of a 75-year-old man in whom a restricted SAH recurred in the cortical sulcus following a huge subcortical hemorrhage. He presented with an unknown restricted SAH in the left frontal sulcus twice before neck clipping for a right IC-PC unruptured aneurysm. Postoperative computed tomography (CT) revealed a recurrent SAH in the left frontal lobe, and it spread gradually. T2(*) weighted imaging (T2(*)WI) revealed subarachnoid hemosiderosis and superficial cortical hemosiderosis in the frontal and parietal lobe. On the 21st postoperative day, he suddenly presented right hemiplegia and a huge subcortical hemorrhage was observed in the left frontal lobe on CT. Emergent removal of the hematoma was performed, but the patient had become bedridden. Pathological diagnosis of CAA was made. A recurrent restricted SAH in the frontal sulcus might have been a warning sign of a huge subcortical hemorrhage. In the aging society, a radiological prediction of CAA is very important. Although it is generally thought to be very difficult, T2(*)WI may be useful for predicting CAA. When we plan surgery for elderly people, we must always take CAA into consideration.

Neurology_Adams

readily corroborated by an unenhanced CT. Of our 26 patients, 14 had normal blood pressure, and in several of the fatal cases there was amyloidosis of the affected vessels; 2 patients were receiving anticoagulants, 2 had an arteriovenous malformation, and 1 had a metastatic tumor. Similarly, in the series of 22 patients with lobar clots reported by Kase and colleagues, 55 percent were normotensive; metastatic tumors, arteriovenous malformations, and blood dyscrasias were found in 14, 9, and 5 percent of the patients, respectively. The role of amyloid angiopathy in lobar hemorrhage in the elderly patient is discussed further on.

List of MeSH codes (C10)

– infarction, middle cerebral artery – infarction, posterior cerebral artery – intracranial aneurysm – intracranial arteriosclerosis – dementia, vascular – intracranial arteriovenous malformations – intracranial arteriovenous malformations – intracranial embolism and thrombosis – intracranial embolism – intracranial thrombosis – sinus thrombosis, intracranial – cavernous sinus thrombosis – lateral sinus thrombosis – sagittal sinus thrombosis – intracranial hemorrhages – cerebral hemorrhage – basal ganglia hemorrhage – putaminal hemorrhage – cerebral hemorrhage, traumatic – intracranial hemorrhage, hypertensive – intracranial hemorrhage, traumatic – brain hemorrhage, traumatic – brain stem hemorrhage, traumatic – cerebral hemorrhage, traumatic – hematoma, epidural, cranial – hematoma, subdural – hematoma, subdural, acute – hematoma, subdural, chronic – hematoma, subdural, intracranial – subarachnoid hemorrhage, traumatic

Stroke

Intracerebral hemorrhage It generally occurs in small arteries or arterioles and is commonly due to hypertension, intracranial vascular malformations (including cavernous angiomas or arteriovenous malformations), cerebral amyloid angiopathy, or infarcts into which secondary hemorrhage has occurred. Other potential causes are trauma, bleeding disorders, amyloid angiopathy, illicit drug use (e.g., amphetamines or cocaine). The hematoma enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the ventricular system, CSF or the pial surface. A third of intracerebral bleed is into the brain's ventricles. ICH has a mortality rate of 44 percent after 30 days, higher than ischemic stroke or subarachnoid hemorrhage (which technically may also be classified as a type of stroke). Other Other causes may include spasm of an artery. This may occur due to cocaine.

[Clinical presentation and surgical indication in intracerebral lobar hemorrhage of elderly patients associated with amyloid angiopathy].

There is controversy concerning the surgical indications for cerebral lobar hemorrhage secondary to amyloid angiopathy in the elderly. We encountered 14 patients with such a lesion, operated on 10 of them, and evaluated their clinical findings and surgical outcome. There were 7 males and 7 females, and their ages ranged from 66 to 87 years (mean age: 75.9 years). Consciousness, CT and surgical findings, and outcome were examined. Nine patients were alert or somnolent and five were semicomatose or comatose. The most common sites of the hemorrhages were the parietal lobe and occipital lobe, and the bleeding was massive, with volume of 28-120 ml. The hematomas were solitary and there had been no previous bleeding. They were evacuated thoroughly by open surgery, and there was difficulty in achieving hemostasis. The arteries in the involved cortex of 6 patients were positive for Congo red staining. There was no rebleeding postoperatively. Five of the six alert or somnolent patients with hematoma volume of 28-60 ml recovered clinically, and their outcome was good. One developed rebleeding four months later at a different site and became bed-ridden. Four of the patients who were semicomatose or comatose and whose hematoma volume 70-120 ml either died or became bed-ridden. Surgery may be indicated in patients with cerebral lobar hemorrhage if their consciousness level in good, but it would be of limited value in elderly patients whose underlying disorder is amyloid angiopathy.

[A 59-year-old woman with recurrent convulsive seizures, cerebral infarctions, dementia, and intracranial calcifications].

A 59-year-old woman with recurrent seizures and progressive dementia is reported. Her past history and familial history were unremarkable. She became short-tempered at 56 years old (Oct. 1991). She had the first seizure attack and was admitted to a hospital at March 4, 1993, with prolonged disturbance of consciousness and subsequent mental deterioration. Her brain CT showed multiple small calcifications in the subcortical white matter and pons. The laboratory data including blood count, serum chemistry, serological studies and CSF was normal. MRI and digital subtraction angiography of the cranial vessels were unremarkable. There was a decrease in accumulation in the right cerebral hemisphere on 123I IMP SPECT. Despite anti-convulsant therapy, she had recurrent seizures several times, with gradual worsening of her mental state. She had the latest seizure attack and was transferred to Matsusaka Chuo Hospital, on August 29, 1993. After the attack she had been in the apallic state, and died on Nov. 13, 1995. This case was discussed in a neurological CPC. The discussants suggested that the isolated angiitis of the central nervous system caused secondary seizures and cerebral infarctions. Post-mortem examination revealed the CNS findings of vasculitis at various stages, calcification or mineralization mainly in the subcortical white matter and pons, massive cerebral infarctions with massive exudate, fresh and old small bleedings and exudate around the inflamed or calcified vessels. The white matter degeneration resembled that of Binswanger leukoencephalopathy. The final pathological diagnosis was isolated angiitis of the central nervous system since there was no inflammatory changes or atherosclerotic change of the blood vessels in the extracranial organs.

[Indications for surgery to determine the etiology of subcortical hemorrhage].

We studied the etiology of subcortical hemorrhage in 55 patients (30 males, 25 females), aged 19-83 years (mean 60 years). CT scan was made in all patients on admission, with the use of intravenous infusion of contrast agent in 35 patients. Cerebral angiography was performed in 37 patients and MRI was performed in 22 patients. Forty-one patients underwent surgery and the other fourteen patients were treated conservatively. The cause of bleeding had been discovered before surgery in 12 cases; 10 arteriovenous malformations and 2 brain tumors. They were discovered by meticulous neuroradiological investigations including cerebral angiography, MRI, dynamic MRI, MRA and enhancing CT. The cause of bleeding was newly discovered after surgery in 7 cases; all of amyloid angiopathy. It remained unknown in the other 22 surgical cases although hypertensive angiopathy was suspected in eleven of them. Among the 14 patients who received conservative therapy, hemorrhagic diathesis including the use of Warfarin and DIC was the cause of bleeding in four cases and the etiology remained unknown in other ten, although hypertensive angiopathy was suspected in eight of them. The 32 patients in whom the etiology remained unknown had been observed as long as 12-120 months (mean, 40 months) and although bleeding has occurred at different locations in two of these patients, there has been no recurrence of bleeding at the same location in any of them. In conclusion, surgery is not indicated to determine the etiology of subcortical hemorrhage when meticulous neuroradiological investigations fail to disclose any vascular or tumorous lesions.

[Cerebral amyloid angiopathy (congophilic angiopathy): a rare cause of massive cerebral hemorrhage. Report of an "age-related" sporadic case].

Cerebral amyloidosis is a form of organ-limited amyloidosis, which doesn't involve any organ other than brain and which comprises several subtypes, including "congophilic angiopathy" (CA), "senile plaques" (SP), "neurofibrillary degeneration" (ND), "stellate amyloid cores" of spongiform encephalopathies. It is found in 5 to around 20% of human population in people aged 60 to 90 years, the increasing being strictly related to ageing. Usually it is associated to SP and occasionally to ND, being distinguished into familial and non-familial (age-related) variants. It affects intracortical and leptomeningeal variously sized vessels of the brain and is a leading pathogenetic factor in determining a rare but possibly even recurrent form of a massive intraparenchymal cerebral hemorrhage, constituting a 0.2 per cent of brain vascular accidents of any origin and a 5-10 per cent if only primary non traumatic brain hemorrhages are considered. A case of non-familial CA in a previously non-demented nor hypertensive female patient aged 65 years is reported on, who was admitted due to an almost abrupt onset of neurologic symptoms mainly dominated by a sudden loss of consciousness together with a left sensory-motor deficiency syndrome. The patient who had been operated on of unilateral mastectomy eight years earlier due to an invasive ductal carcinoma of the breast was found affected by a devastating brain hemorrhage in the right temporo-occipital lobes with subsequent deflection of the brainstem axis toward the opposite side detected by means of CT/MRI and angiographic investigations.(ABSTRACT TRUNCATED AT 250 WORDS)

[Clinical evaluation of subarachnoid hemorrhage of unknown etiology].

This study concerns 16 cases with spontaneous subarachnoid hemorrhage (SAH) of unknown etiology experienced in our department during a period from September 1979 through August 1986. SAH was confirmed by computed tomographic scanning (CT) or lumbar puncture. All cases were studied by four or three-vessel study. In the case of three-vessel study, adequate opacification of the posterior inferior cerebellar artery contralateral to the injected vertebral artery was considered as a necessary condition. Panangiography was repeated in all patients one to two weeks after the initial study and was negative. The severity of SAH in these patients on admission was relatively mild (Hunt and Kosnik grade I + II = 75%), and the degree of subarachnoid bleeding on CT was also mild. Medium to long-term outcome was excellent or good in 81% of cases, and none of them experienced rebleeding. Only one patient died of severe vasospasm on the 20th hospital day, but no aneurysm was found at autopsy. Illustrative 3 patients in whom the cause of SAH had been finally found was briefly reported. In the first patient, SAH was secondary to a paraventricular cryptic angioma. In the second patient, a microaneurysm had been concealed at the initial angiography by the parent arteries or intra-aneurysmal clot. In the third case of a fusiform aneurysm of the vertebral artery, the aneurysm proximal to the posterior inferior cerebellar artery could not be found at the first three-vessel angiography. Importance of CT and the necessity of repeat panangiography including magnification or oblique views so as not to over-look the causative vascular abnormalities were emphasized.