STRIATOCAPSULAR HEMORRHAGES

The striatocapsular region comprises the lenticular and caudate nuclei, the internal capsule, and the external capsule and subinsular area. The presentation and prognosis of striatocapsular hemorrhages depend on the epicenter of the bleeding. Chung and colleagues have proposed a detailed classification that divides these hemorrhages into six types, as listed in Table 10-1.²⁴

TABLE 10-1 Anatomical classification of striatocapsular hemorrhages.

Most putaminal hemorrhages encountered in practice tend to be lateral and remain localized in the region of the lenticular nucleus or expand toward the insula. Medial hemorrhages occur less often, and, when large, they may be difficult to differentiate at first glance from external thalamic hematomas. Massive hemorrhages may obscure the center of origin and extend both medially and laterally; herniation is often present early.

Impaired level of consciousness at presentation and large hematoma size consistently predict poor functional outcome in patients with striatocapsular hemorrhage. Additionally, hydrocephalus and intraventricular extension are markers of large hematoma size in patients with putaminal hemorrhage (unlike in those with bleedings emanating from the caudate) and thus also forecast death or dependency.^21–23 Capsular involvement is strongly associated with persistent hemiparesis, but weakness tends to be severe only in patients with larger hematomas.

Lateral Putaminal Hemorrhage

Case Vignette

A 48-year-old Hispanic woman with recent diagnosis of hypertension presented with sudden onset of headache and left-sided weakness. Examination revealed an alert patient with a blood pressure of 210/124 mm Hg, mild right horizontal gaze palsy, and severe left hemiparesis. She appeared relatively unconcerned about her weakness and paid less attention to activity occurring over her left visual field. The patient had no complications during her acute hospitalization. Her CT scan of the brain revealed a right lateral putaminal hemorrhage, later confirmed on MRI (Figure 10-3, upper two rows). No underlying vascular anomalies or masses were found. Six months later, she had residual weakness but recovered the ability to walk independently with minimal support and had partial functional use of her left arm. Follow-up imaging is shown in the lower row of Figure 10-3.

Figure 10-3 Computed tomography scan of the brain showing a lateral putaminal hemorrhage of moderate size exerting mild mass effect over the lateral ventricle. The hypodense rim surrounding the hematoma represents edema (A). Magnetic resonance imaging (MRI) shows that the hemorrhage is isointense on T1-weighted sequence (B) and hyperintense on T2-weighted sequence (C), denoting the acuteness of the lesion. Note that edema is better delineated by MRI. Gradient-recalled echo (GRE) shows the acute hemorrhage as a dark signal, whereas edema appears bright as in T2-weighted images (D). Six months later, repeat MRI shows a relatively small, linear residual scar seen on T1-weighted (E) and GRE images (F).

♦ Lateral striatocapsular hemorrhages are lens-shaped lesions that remain typically contained within the deep brain parenchyma; thus they are not readily accessible for surgical drainage.

♦ Although often deemed putaminal in origin, these hemorrhages typically arise from rupture of lateral lenticulostriate branches into more lateral structures (external capsule, claustrum) and may actually spare the putamen itself when not large.

♦ Most patients have preserved or minimally impaired level of consciousness. The severity of weakness depends on extension into the posterior limb of the internal capsule. Some degree of dysphasia is seen in nearly half of the cases with hematomas in the dominant hemisphere but is usually transient. Neglect and anosognosia can occasionally be observed in patients with hemorrhages in the nondominant side, and they also tend to improve rather rapidly in most cases. Mild to moderate conjugate gaze paresis may be present in the acute phase.²⁴

♦ These hematomas can rarely rupture into the anterior horn of the lateral ventricle.

♦ They exert pressure on more medial structures, and their expansion may cause subfalcine herniation.

♦ Good functional recovery can be expected in the majority of cases.

Massive Striatocapsular Hemorrhage

♦ Massive hemorrhages may occur at onset or develop after hematoma growth in the first few hours following the original bleeding (Figure 10-4).

♦ Patients with massive striatocapsular hemorrhage present with stupor or coma, contralateral hemiplegia, and marked ocular movement abnormalities. Signs of subfalcine and transtentorial (diencephalic or uncal) herniation are obvious on initial examination or appear shortly after.

♦ Ventricular extension is characteristically present, and hydrocephalus (often in the form of trapping of the contralateral ventricle) is a frequent complication.

♦ Outcome is typically poor, with high rates of mortality.

♦ There is no evidence that surgical evacuation improves outcome.²⁵

Figure 10-4 A 68-year-old woman with history of hypertension presented with coma and right-sided hemiparesis. Her computed tomography scan of the head showed a massive putaminal hemorrhage invading the anterior horn of the lateral ventricle and producing mass effect with midline shift and early subfalcine herniation.

Posterolateral Striatocapsular Hemorrhage

♦ Posterolateral striatocapsular hemorrhages, the most common type of striatocapsular hemorrhage, primarily affect the posterior putamen and tend to spread ventrally or dorsally (Figure 10-5). However, rostrocaudal extension may also occur and produce mass effect over diencephalic structures.

♦ Patients are most commonly awake but hemiparetic because of frequent involvement (direct or indirectly by compression) of the posterior limb of the internal capsule. Transient dysphasia or neglect and gaze deviation (ipsilateral or, rarely, “wrong way”) may be present. Sensory deficits are relatively frequent.

♦ Intraventricular extension occurs very rarely.

♦ In the absence of enlargement, death is exceptional, but functional recovery is often limited because of persistent hemiparesis.

Figure 10-5 A 65-year-old man with history of hypertension presented with lethargy and right-sided hemiparesis. Initial computed tomography (CT) scan of the head (left and middle) showed a large left posterolateral putaminal hemorrhage with expansion into the ipsilateral temporal lobe. After craniectomy, a repeat CT scan confirmed successful hematoma evacuation (right). The patient had good clinical outcome.

Middle-Posteromedial Striatocapsular Hemorrhage

♦ Middle striatocapsular hemorrhages are relatively uncommon and arise from rupture of middle lenticulostriate branches. Posteromedial striatocapsular hemorrhages may be caused by rupture of terminal branches of the anterior choroidal artery.

♦ Patients are most often alert and may present with abnormal ocular movements and mild to moderate hemiparesis.

♦ They usually spread laterally toward the lateral aspect of the lenticular nucleus and the external capsule (Figure 10-6).

♦ Large hemorrhages with epicenter in the globus pallidus or the medial putamen may be indistinguishable from hematomas originating from the lateral portions of the lenticular nucleus.

♦ Ventricular rupture is distinctly infrequent.

♦ Functional prognosis tends to be good to fair, with more than half of patients recovering independence.²⁴

Figure 10-6 A 72-year-old hypertensive man presented with sudden onset of right sided hemiparesis. Head computed tomography scan revealed a left middle striatocapsular hemorrhage with typical lateral extension. Notice the medial putaminal epicenter of the hematoma without rupture into the lateral ventricle.

Caudate Hemorrhage

♦ Hemorrhages arising from the head or body of the caudate constitute the anterior group of striatocapsular hemorrhages and are caused by rupture of the recurrent artery of Heubner.

♦ Caudate hemorrhages are invariably associated with intraventricular hemorrhage (Figure 10-7).

♦ They represent an obligatory differential diagnosis in any case of intraventricular hemorrhage.

♦ Hematoma volume tends to be relatively small to moderate.

♦ Patients present with sudden severe headache and neck stiffness but usually have only mild neurological impairment. Memory problems, abulia and perseveration, or, less frequently, restless agitation may be noted during the first few months but later tend to resolve. Larger hematomas may produce focal deficits in the acute phase that are most often mild and transient.

♦ Functional outcome is characteristically favorable.^24,26

Figure 10-7 A 62-year-old woman with history of diabetes and hypertension developed a sudden, severe headache and presented in the emergency department with a blood pressure of 260/100. Computed tomography scan of the head showed a left caudate hemorrhage with extension into the left lateral ventricle.

LOBAR HEMORRHAGES

Lobar spontaneous IPH may be less frequent than is traditionally estimated. In recent years, enhanced technology, mainly in the form of MRI and highly improved angiographic equipment, has demonstrated that cases previously believed to be due to hypertension are actually caused by other conditions, such as occult vascular anomalies, venous thrombosis, or, most often, amyloid angiopathy. Secondary causes of IPH are discussed in the next chapter but must be carefully excluded before concluding that a lobar hemorrhage is spontaneous even in a hypertensive patient (Table 10-2). Neuroimaging is an extremely valuable and in fact irreplaceable tool to recognize the correct etiology of bleeding in patients with lobar IPH.

TABLE 10-2 Causes of lobar intracerebral hemorrhage other than primary arterial hypertension

AVM, arteriovenous malformation; CSF, cerebrospinal fluid; CT, computed tomography; DWI, diffusion-weighted imagery; GRE, gradient-recall echo; MRI, magnetic resonance imaging; TEE, transesophageal echocardiography.

Lobar hemorrhages tend to originate from the cortical-subcortical or gray-white matter junction and extend into the adjacent white matter. Any lobe can be involved, and the location and laterality of the hematoma determines the clinical manifestations. Seizures, typically of focal onset with secondary generalization, occur frequently occur at onset and during the acute phase.^27,28 Multiple hemorrhage locations, simultaneous or sequential, may occur because of hypertension but must be regarded as a potential indicator of an alternative cause (mainly amyloid angiopathy in the elderly with cortical hemorrhages or cavernous malformations in young patients with deep hemorrhages).

The overall outcome of patients with lobar IPH is deemed to be comparatively more favorable than after ganglionic hemorrhages.^29,30 Once again, one has to be cautious when analyzing older series reporting favorable outcomes because they may have included patients with more benign secondary hemorrhages in the group of spontaneous lobar IPH. Size is still the most powerful predictor of outcome, and intraventricular extension remains a prognosticator of reduced chances of survival and poor recovery.

Hematoma Expansion

Case Vignette

A 74-year-old African American man with long history of hypertension and poor compliance with prescribed antihypertensive medications was brought to the emergency department after being found wandering and limping on the street. Upon arrival, the patient’s blood pressure was 186/126 mm Hg. Neurological examination showed that he was confused and had scant verbal output, right gaze preference with decreased response to visual threat on the left, left hemiplegia, and left hypoesthesia. The degree of weakness had worsened in comparison with the first examination by the paramedics. CT scan showed a right frontoparietal hematoma (Figure 10-8, left) On the second hospital day, the patient was noticed to be slightly more lethargic but otherwise unchanged; repeat CT showed mild increase in the regional mass effect. In the morning of the third day, he became comatose because of massive hematoma enlargement (Figure 10-8, right). His brainstem reflexes were present, but he only responded with extensor posturing to maximal pain. After discussion with the family, further care was limited to comfort measures, and the patient expired hours later.

Figure 10-8 Head computed tomography (CT) scan showing a right frontoparietal hematoma of moderate size (left). Repeat CT scan obtained after clinical decline revealed massive hematoma enlargement with pronounced midline shift and hydrocephalus (right).

♦ The only manifestation of early hematoma expansion in patients with lobar hemorrhages in certain locations may be mild depression in the level of consciousness.

♦ Although most cases of hematoma growth occur within the first 24 hours, this complication is possible at later times. Also, the risk of worsening mass effect from the accompanying edema subsists for much longer.³¹

♦ Serial imaging is indicated for at least the first 72 hours, and at later times depending on clinical evolution, to follow patients with moderate or large lobar hematomas.

♦ Hematoma growth is independently associated with increased risk of death and poor functional outcome.³²

♦ Patients with substantial hematoma growth causing neurological deterioration may be successfully treated with surgical intervention;³³ meaningful recovery is possible when the patient has rehabilitation potential. Early recognition of the hematoma expansion by timely imaging studies is therefore essential.

Hydrocephalus

♦ Large lobar hematomas can produce obstructive hydrocephalus by compressing the foramen of Monro, thus trapping the contralateral ventricle (Figure 10-9).

♦ Because ventricular drainage may exacerbate the pressure gradient, presence of hydrocephalus is sometimes regarded as a relative indication for surgical evacuation in cases with accessible hematomas and extensive mass effect.

Figure 10-9 A 70-year-old man with history of hypertension who presented with lethargy, seizures, and left-sided hemiparesis. Head computed tomography scan disclosed a large right frontal lobar hemorrhage obliterating the right lateral ventricle and causing midline shift and early trapping of the left lateral ventricle.

Temporal Hematomas

♦ Hematomas located in the temporal lobe represent highly unstable situations and must be considered a major threat of herniation for at least 2 weeks after the onset of the hemorrhage (Figure 10-10).

♦ Surgery may be lifesaving in cases of impending herniation, and serial imaging may guide the appropriate surgical timing before signs of herniation have already developed.

Figure 10-10 A 66-year-old right-handed man with history of hypertension developed sudden onset of receptive aphasia and right-sided hemiparesis and rapidly became poorly responsive. Computed tomography scan of the brain showed a large left temporal lobe hemorrhage exerting pronounced mass effect on the diencephalon. Notice the effacement of the perimesencephalic cistern and contralateral hydrocephalus.

Focal Lobar Hemorrhage

♦ Benign-appearing, focal lobar hematomas must be carefully investigated for causes other than hypertension.

♦ In older patients, the diagnostic investigation must include an MRI with gadolinium (although tumors are typically associated with extensive vasogenic edema disproportionate to the size of the hematoma itself) and a GRE sequence to rule out previous cortical hemorrhages suspicious for amyloid angiopathy (Figure 10-11).

♦ In younger patients, cerebral venous thrombosis and cavernous angiomas must be excluded using MRI and MR venography (venous phase of catheter angiography may be necessary for confirmation of venous thrombosis).

♦ Cortical venous thrombosis is difficult to diagnose with certainty and cannot be totally excluded even after documenting a normal venography.

Figure 10-11 A 48-year-old woman with history of hypertension presented with right-sided sensory loss. Head computed tomography scan showed a focal left parietal hemorrhage (left). Gradient-recall echo sequence of the magnetic resonance imaging during the acute stage displayed low signal intensity representing deoxyhemoglobin (right).

Surgical Evacuation (Figure 10-12)

♦ Serial imaging is indicated in patients with lobar hematomas, especially when located in relatively noneloquent brain areas where hemorrhage may grow without major additional clinical changes.

♦ Superficially seated hematomas may be evacuated surgically without producing any additional damage to healthy brain (Figure 10-12).

♦ Although surgery has not been shown to improve outcome in patients with intracerebral hemorrhage at large,³⁴ there is some evidence that early surgery might be beneficial in the subgroup of patients with superficial hematomas.²⁵

Figure 10-12 A 56-year old man with history of hypertension presented to the emergency department with acute onset of headache and was found to have left homonomous hemianopia. His head computed tomography (CT) scan showed a large lobar hemorrhage extending from the cortex into the subcortical white matter (left and middle). The patient underwent surgical evacuation. Postoperative CT scan demonstrates successful hematoma removal (right).

THALAMIC HEMORRHAGES

The thalamus is a complex structure comprising multiple relay nuclei with distinct functions. Nuclear groups also differ in their arterial supply and may harbor anatomically confined hemorrhages that produce fairly consistent clinical syndromes based on their precise primary location. Functional outcome mainly depends on the size of the hematoma and whether extension into the lower diencephalon and midbrain occurs.³⁵ Hematoma diameter greater than 3 cm is associated with high mortality rate,^36,37 whereas volumes less than 10 cc often foretell favorable recovery. Unlike what is seen with most other hemorrhages, ventricular extension is compatible with good outcome in patients with thalamic bleeding.^36,38 In fact, patients with medial thalamic hemorrhages may benefit from decompression into the ventricular space, thus avoiding the dangerous caudal spread into the midbrain. However, when ventricular extension is accompanied by hydrocephalus the prognosis worsens substantially.^36,38,39

Careful analysis of neuroimaging findings has allowed the development of a clinic-anatomical classification that divides thalamic hemorrhages into five types, as listed in Table 10-3.³⁹

TABLE 10-3 Anatomical classification of thalamic hemorrhages.

Global Thalamic Hematomas

Case Vignette

A 66-year-old African American man with background of hypertension and diabetes type 2 developed sudden headache and vomiting shortly after waking up. Initially conscious, he rapidly became less responsive. Upon arrival to the emergency department, the patient had a Glasgow coma scale sum score of 6; he exhibited small sluggishly reactive pupils and forced gaze deviation to the left and downward. His blood pressure was 198/122 mm Hg, and he had hyperpnea. CT scan showed a massive thalamic hemorrhage with intraventricular extension causing severe hydrocephalus (Figure 10-13). Emergency ventriculostomy failed to improve his clinical status. After discussing the ominous prognosis with the patient’s family, intubation was withheld. A short hospitalization was complicated by aspiration pneumonia and sepsis, and the patient was subsequently discharged in persistent coma to a hospice.

Figure 10-13 Computed tomography scan shows massive thalamic hemorrhage with severe obstructive hydrocephalus due to obliteration of the third ventricle. Note downward (upper left) and upward (lower left and right) extension of the hematoma.

♦ Global thalamic hemorrhages usually cover the whole area of the thalamus and extend beyond its boundaries to involve adjacent structures: the internal capsule posteriorly, the lenticular nucleus laterally, the white matter of the corona radiata rostrally, and the midbrain caudally. Midline shift and obstructive hydrocephalus, often massive, occur frequently.

♦ Most patients present with stupor or coma, severe sensory and motor deficits, and ocular abnormalities. The classical ocular findings consist of paralysis of upward gaze, resulting in deviation of the eyes downward and inward “as if peering down at the nose.”⁴⁰ Pupils tend to be miotic (particularly the ipsilateral to the side of the hematoma) and poorly reactive to light. Convergence is also impaired, and attempts to converge may elicit nystagmoid jerks. Most clinical manifestations are caused by involvement of the tectum of the mesencephalon.

♦ Fatal outcome is announced by the appearance of signs of central (diencephalic) herniation, including midposition nonreactive pupils, abnormal posturing, and central hyperventilation. These patients do not develop signs of uncal herniation (i.e., they do not exhibit a “blown pupil”).

♦ Mortality occurs in three quarters of these patients, and survivors achieve only limited recovery.

♦ Figures 10-14 and 10-15 are additional examples of massive thalamic hemorrhages.

Figure 10-14 A 66-year-old man with history of uncontrolled hypertension presented with coma, downward eye deviation, and right-sided hemiparesis. Computed tomography scan showed a global thalamic hemorrhage with invasion of the anterior horn, third ventricle, and mesencephalon (left). Lower cut demonstrates tonsillar herniation indicated by the arrows (right).

Figure 10-15 A 53-year-old man with history of refractory hypertension presented with sudden onset of headache and left hemiplegia followed by rapid deterioration to coma. His computed tomography scan showed global thalamic hemorrhage with multidirectional expansion including intraventricular hemorrhage (left). Additionally, the same scan disclosed a rare simultaneous pontine hemorrhage indicated by the arrow (right).

Anterior Thalamic Hemorrhage

♦ This is the least common type of thalamic hemorrhage.

♦ Usually hemorrhage size is small or moderate, remaining confined to the anterior aspect of the thalamus or extending into the anterior capsular limb and, at most, the posteromedial margins of the caudate (Figure 10-16).

♦ It may sometimes drain into the frontal horn of the lateral ventricle but without producing hydrocephalus.

♦ Level of consciousness is normal, but patients often exhibit abulia, apathy, and indifference. Impairment of short-term memory may be persistent. Sensory and motor deficits are typically minor and transient.

♦ Functional outcome is typically favorable.³⁹

Figure 10-16 A 62-year-old woman with history of hypertension presented with headache and acute confusion. Her head computed tomography scan showed an anterior thalamic hemorrhage with medial extension. Note the high anterior location and early expansion into the anterior horn of the lateral ventricle.

Posteromedial Thalamic Hemorrhage

♦ Posteromedial (or simply medial) hematomas may be small and localized, but larger hematomas extend caudally, damaging the upper midbrain, medially compressing the third ventricle, and provoking massive hydrocephalus (Figure 10-17).

♦ Even small hemorrhages can generate long-lasting memory and behavioral problems.^41,42 Focal deficits are uncommon in these cases. Minor ventricular invasion without hydrocephalus does not affect the prognosis unfavorably.

♦ Hematomas associated with mesencephalic compromise and hydrocephalus carry poor prognosis, regardless of the total size.³⁹

Figure 10-17 A 55-year-old man presented with coma, “wrong-way” eye deviation, and left-sided weakness. Initial computed tomography (CT) scan showed a posteromedial thalamic hematoma with medial-caudal extension into the right cerebral peduncle (left). A second CT scan obtained hours later revealed mild expansion of the hematoma and placement of emergent ventriculostomy due to early hydrocephalus (middle). Ten days later, a repeat CT scan showed the evolution of the hematoma with surrounding edema (right).

Posterolateral Thalamic Hemorrhage

♦ This is by far the most common type of thalamic hemorrhage, accounting for one half to three quarters of all cases.^37,39

♦ They tend to spread into the posterior limb of the internal capsule and the medial lenticular nucleus (Figure 10-18); this extension is responsible for the presence of hemiparesis. Dystonic postures (“thalamic hand”) and choreiform adventitious movements can also be observed in these cases.

♦ The most characteristic manifestations are contralateral hypoesthesia occasionally accompanied by disturbing or frankly painful dysesthesias. Ipsilateral Horner’s syndrome is another possible finding. Variable degrees of dysphasia, dyspraxia, and hemineglect may also be observed.^39,43 Other cognitive and behavioral abnormalities are infrequent.

♦ Recovery tends to be partial, and the mortality rate is 30%.³⁹

Figure 10-18 Two examples of posterolateral thalamic hemorrhages. Both patients presented with left hemibody sensory and motor loss. Both computed tomography (CT) scans show a thalamic hemorrhage with characteristic rupture into the posterior horn of the lateral ventricle. The CT scan on the right represents a larger hematoma with extension into the lentiform nucleus and posterior limb of the internal capsule, and some degree of midline shift.

Dorsal Thalamic Hemorrhage

♦ Dorsal hemorrhages are usually situated alongside the body of the lateral ventricle (Figure 10-19). They tend to be of medium size and expand into the white matter tracts of the corona radiata.

♦ Sensorimotor manifestations may resemble a lacunar syndrome.

♦ Ventricular extension is infrequent and benign.

♦ Initial focal deficits tend to resolve over time, and outcome is characteristically favorable.

Figure 10-19 A 55-year-old hypertensive man presented with left hemibody paresthesia and had sensory loss on examination. His head computed tomography scan revealed a right dorsal thalamic hemorrhage with pulvinar involvement and internal capsule extension (left). Notice also the upward extension into the right lateral ventricle (right).

PONTINE HEMORRHAGES

Before the introduction of CT, pontine hemorrhages were thought to be nearly always fatal. However, modern brain imaging has taught us that not only survival but also meaningful and sometimes fairly complete recovery is possible after bleeding in the pons. The question is how often spontaneous (hypertensive) pontine hemorrhages are followed by a favorable course, because evidence of cavernous angiomas is often found on MRI of patients with benign evolution. Thus CT allowed us to recognize the greater spectrum of prognosis in patients with pontine hemorrhages, and MRI is showing us that cause is the most important predictor of outcome in these patients.⁴⁴ In practice, patients with nonmassive pontine hemorrhage and a favorable clinical evolution should undergo MRI to exclude cavernous angiomas, particularly when they are young and have no previously documented hypertension.

Prognosis is highly dependent on clinical severity at presentation, but radiological signs including hydrocephalus, larger hemorrhage size, and extension into the midbrain and thalamus are also reliable prognosticators of poor outcome.^45–47 Conversely, patients with small hematomas (< 4 cc) restricted to the tegmentum tend to have minor neurological sequelae.^46,48 Hemorrhage location serves as the foundation for a CT classification with useful prognostic implications (Table 10-4).⁴⁸

TABLE 10-4 Types of pontine hemorrhage.

Massive Pontine Hemorrhage

Case Vignette

An adult man of unknown identity was found face down on the street, unconscious and surrounded by vomit. He was emergently intubated by paramedics and transported to the emergency department. On arrival, his vital signs revealed hypertension (190/100 mm Hg), sinus tachycardia (115 bpm), and hyperthermia (101°F). He was comatose and had 3-mm nonreactive pupils, absent corneal reflexes, and minimal oculocaloric response to irrigation of the right ear. There was no motor response to pain. CT scan disclosed a massive pontine hemorrhage (Figure 10-20). Over the following hours, the patient lost all signs of brainstem function and, after formal demonstration of apnea on the apnea test, he was declared brain dead.

Figure 10-20 Computed tomography scan shows a massive pontine hemorrhage with compression and invasion of the fourth ventricle (arrows).

♦ Massive pontine hemorrhages occupy the whole pons, compress the fourth ventricle producing obstructive hydrocephalus, and extend upward into the midbrain and diencephalon (Figures 10-20 and 10-21).

♦ Patients present with coma, miotic pupils, absent corneal and oculocaloric reflexes, and quadriplegia or extensor posturing. Hyperthermia and tachycardia are common and portend fatal outcome.⁴⁷

♦ They probably originate from rupture of paramedian or short circumferential vessels.

♦ Treatment of hydrocephalus is probably irrelevant.

♦ Fatality rate exceeds 90%.^46,48

Figure 10-21 A 48-year-old man with history of untreated hypertension was brought comatose to the emergency department. Computed tomography scan shows a massive pontine hemorrhage with obliteration of the fourth ventricle (left), hydrocephalus (middle), and upward spread into the midbrain and diencephalon (right).

Bilateral Tegmental Hemorrhage

♦ Pontine hemorrhages that are not massive but cross the midline (Figure 10-22) are typically associated with better survival but considerable neurological impairment.

♦ Midbrain and intraventricular extension occur often, but severe hydrocephalus is less frequent.

♦ They originate from rupture of paramedian or short circumferential vessels.

♦ The more ventral the location (basal-tegmental), the worse the prognosis.⁴⁶

♦ Fatality rate is 20% to 55%.^45,46

Figure 10-22 Two cases of bilateral, basal-tegmental pontine hemorrhages. (Left) A 54-year-old woman presented with stupor, small reactive pupils, and withdrawal to pain. Her head computed tomography (CT) scan revealed bilateral tegmental pontine hemorrhage involving the middle cerebellar peduncles. She survived but remained dependent. (Right) A 61-year-old hypertensive man presented with coma, pinpoint pupils, left extensor posturing, and right hemiplegia. His CT scan showed a basal-tegmental pontine hemorrhage, larger on the left. He expired 48 hours later.

Unilateral Tegmental Hemorrhage

♦ Hemorrhage is restricted to one side of the dorsal aspect of the pons with transverse diameter usually smaller than 30 mm and volume less than 3 cc (Figure 10-23).^46,48

♦ When transverse diameter is less than 20 mm, functional prognosis is favorable except in isolated cases with pupillary abnormalities or hydrocephalus.⁴⁵

♦ Patients with ventral extension may develop persistent hemiparesis.

♦ Patients should undergo MRI to investigate for cavernous angiomas, especially if young and without previous history of hypertension.

♦ Survival is the rule.^45,46,48

Figure 10-23 A 74-year-old woman with uncontrolled hypertension and diabetes presented with mild lethargy, right esotropia with one-and-a-half syndrome, right facial palsy, and mild right dysmetria. As indicated by the arrows, computed tomography scan (left) disclosed a small right dorsal tegmental hemorrhage confirmed by magnetic resonance imaging/gradient-recall echo (right). The patient recovered well except for persistent diplopia.

CEREBELLAR HEMORRHAGES

Cerebellar hemorrhages differ fundamentally from other forms of IPH in that timely surgery can lead to dramatic recovery of function and result in meaningful recovery. Noncomatose patients with hemispheric cerebellar hematomas typically present with inability to walk, as well as headache, vomiting, and dizziness. Appendicular ataxia without hemiplegia (although variable degrees of hemiparesis may be present) and dysarthria are common expressions of cerebellar dysfunction. Compression of the pons is typically manifested by peripheral facial palsy and ipsilateral horizontal gaze palsy. Appearance of these pontine signs may herald subsequent depression in the level of consciousness, but sudden coma may develop unannounced after a seemingly benign initial course.^49,50

Neuroimaging modalities allow early diagnosis and recognition of underlying causes. Furthermore, radiological findings often play a crucial role in the determination of the timing of surgery. In fact, the unpredictable clinical evolution of cerebellar hemorrhages and potentially fatal consequences of sudden deterioration due to brainstem compromise make serial imaging an invaluable tool in the management of these critical patients.

The differential diagnosis of hemorrhagic masses in the cerebellum is extensive and includes spontaneous hematomas, drug-induced hemorrhages (anticoagulants, thrombolytics), arteriovenous malformations (AVMs), tumors (metastasis, hemangioblastomas), traumatic lesions, and blood dyscrasias.

Most spontaneous cerebellar hemorrhages originate from one of the dentate nuclei, likely from rupture of a distal branch of the superior cerebellar artery or occasionally the posterior inferior cerebellar artery. Invasion of the fourth ventricle and compression of the pontine tegmentum are frequent complications of these cerebellar hemisphere hemorrhages. The relatively infrequent vermian hemorrhages must be distinguished because of their poorer prognosis. They are almost always associated with fourth ventricular hemorrhage and often extend directly into the pontine tegmentum bilaterally.

Large Cerebellar Hematomas with Surgical Decompression

Case Vignette

A 56-year-old man with history of hypertension and coronary artery disease presented with sudden onset of headache, dizziness, and inability to walk. On examination, he was fully lucid, and his blood pressure was 185/110 mm Hg; his neurological deficits were a very mild right peripheral facial palsy, slight right hemiparesis, right dysmetria, and pronounced gait ataxia. Brain imaging showing a large hematoma in the right cerebellar hemisphere is presented in Figure 10-24. Within 8 hours of admission to the ward, the patient became confused and then lethargic, and developed right sixth nerve palsy and right facial paralysis. Emergency surgical evacuation through suboccipital craniotomy was followed by good functional recovery. Postsurgical CT scan is shown in Figure 10-24, lower right. Six months later, the patient had returned to his regular activities as a hospital administrator and complained only of mild balance problems and some slowing of his executive abilities.

Figure 10-24 Computed tomography (CT) scan showing a large (> 3 cm in diameter) right cerebellar hematoma exerting considerable mass effect on the fourth ventricle and the dorsal aspect of the pons with effacement of the peripontine cisterns (upper left). There is also hydrocephalus (arrows), tight posterior fossa and obliteration of the ambient cisterns (arrowheads) as a consequence of upper herniation (upper right). Magnetic resonance imaging/gradient-recall echo shows extensive associated edema (lower left). Postoperative CT scan (lower right) demonstrates successful decompression with reopening of the fourth ventricle.

♦ Radiological variables predictive of neurological decline and requirement of surgery include hematoma diameter 3 cm or larger, obstructive hydrocephalus, ventricular extension, midline location, obliteration of the fourth ventricle, effacement of the quadrigeminal cistern (indicating upward herniation of the vermis into the tentorial notch), and brainstem distortion (Figures 10-25 and 10-26).^50–55 Markers of a “tight posterior fossa” with upward herniation may be more reliable than hematoma size itself for the prediction of neurological deterioration.^51,54,55

♦ Neurological decline occurs in nearly half of all patients with cerebellar hematomas⁵⁰ and tends to develop within the first 36 to 48 hours.⁴⁹

♦ Current guidelines recommend emergent surgical removal of the clot in patients with hematomas greater than 3 cm who are deteriorating and those who have signs of brainstem compression or obstructive hydrocephalus.¹⁰ This recommendation is based on data from nonrandomized cohort studies^34,56,57 and extensive collective experience.

♦ Although comatose patients (at presentation or after decline) can exceptionally survive and achieve meaningful functional recovery after decompressive surgery,^58,59 the prognosis becomes extremely poor when coma is present.^49–51

♦ Overall mortality rate of patients with cerebellar hematomas may reach 40%.

Figure 10-25 A 56-year-old man with history of hypertension presented with acute right sided ataxia. Computed tomography (CT) scan showed a hemorrhage in the right cerebellar hemisphere (left). The next day, the patient became stuporous and developed ipsilateral horizontal gaze and facial palsy. Repeat CT scan revealed significant hematoma expansion with obliteration of the cerebello-pontine cistern and fourth ventricle (middle). He underwent surgical decompression with successful evacuation of the hematoma (right) and good clinical recovery.

Figure 10-26 A 62-year-old woman with history of hypertension presented with sudden headache and left-sided ataxia. Her initial computed tomography (CT) scan (left) showed a large left cerebellar hemispheric hemorrhage (4.5 cm in maximal diameter). She worsened within the next 24 hours and underwent emergency surgery. Postoperative CT scan confirms successful hematoma evacuation (right). She achieved fair functional recovery.

Benign Hemispheric Cerebellar Hemorrhages

♦ Patients with hemispheric cerebellar hematomas less than 3 cm in maximal diameter and no associated hydrocephalus or fourth ventricular extension tend to follow a favorable course without requiring surgical intervention⁵² (Figure 10-27).

♦ However, there is no individual variable or set of indicators that can predict clinical evolution with certainty. For example, patients with hematomas larger than 3 cm in diameter but no compression of the fourth ventricle may have better prognosis than smaller clots producing ventricular obliteration.⁵¹

♦ Thus all patients with cerebellar hemorrhage must be monitored very closely with serial physical and radiological examinations for at least the first 3 to 4 days.

♦ Patients with deterioration in the level of consciousness or new signs of brainstem compression should undergo emergency surgical intervention. Several authors have advocated preemptive surgery in the presence of effacement of the quadrigeminal cisterns or obliteration of the fourth ventricle;^51,54 however, surgical indication based solely on radiological findings remains debatable.

♦ CT or MRI must be carefully evaluated for the possibility of an underlying cause other then hypertension. Helpful diagnostic clues are discussed in the next chapter.

Figure 10-27 A 55-year-old man with a history of hypertension presented with acute occipital headache and vertigo. His computed tomography (CT) scan of the brain (left) showed a small left cerebellar hematoma without significant mass effect. Repeat CT scan performed 45 days later (right) displays complete resolution of hematoma.

Vermian Hemorrhages

♦ Midline cerebellar hemorrhages are infrequent, but their importance lies in their catastrophic outcome.

♦ Patients often present with coma and bilateral ophthalmoplegia caused by direct extension of the hemorrhage into the midline tegmental structures of the pons.

♦ Compression and invasion of the fourth ventricle account for the almost invariable presence of obstructive hydrocephalus (Figure 10-28).

♦ Midline hemorrhages with relatively favorable presentation and evolution should raise the suspicion of a secondary cause.

♦ Mortality and morbidity of spontaneous vermian hematomas approach those of bilateral tegmental pontine hemorrhages.

Figure 10-28 A 40-year-old hypertensive man presented with a severe headache, nausea and vomiting, and truncal ataxia. His computed tomography scan (left) disclosed a midline cerebellar vermian hemorrhage, as marked by the arrows. Notice incipient dilatation of the temporal hems of the lateral ventricles due to obstructive hydrocephalus. Gradient-recall echo sequence of his magnetic resonance imaging (right) showed low signal localized to the vermis with superior vermian cistern extension.

INTRAVENTRICULAR HEMORRHAGES

Hemorrhages primarily located in the ventricular system are most frequently due to underlying causes, such as vascular anomalies (AVM, cavernous angiomas, or, rarely, aneurysms that may be mycotic), coagulation disorders (from blood dyscrasias; iatrogenic, such as following thrombolysis), trauma (including manipulation of a ventriculostomy catheter), and tumors (papilloma, subependymoma, astrocytoma, metastasis, etc.); much less often, they may be spontaneous (with the exception of germinal matrix hemorrhages in premature newborns). We have also seen cases of pure intraventricular hemorrhage in patients with moyamoya-like disease. This classification excludes parenchymal hypertensive hemorrhages with secondary extension into the ventricular space, which largely represent the most common cause of intraventricular clots. The distinction becomes challenging when the parenchymal hematoma is difficult to visualize, as is usually the case with caudate hemorrhages. When the cause of intraventricular hemorrhage remains obscure, the patient should be studied with contrast MRI and conventional angiography. An example of spontaneous intraventricular hemorrhage is presented in Figure 10-29.

Figure 10-29 A 58-year-old woman with history of hypertension and poor compliance with medications presented to the emergency department complaining of severe right-sided headache. Her computed tomography scan showed intraventricular hemorrhage in the right lateral ventricle. Subsequent four-vessel digital subtraction angiogram did not show any evidence of aneurysm or vascular malformation.

Prognosis depends on the clinical severity at presentation and underlying cause of the bleeding.⁶⁰ Coma from onset in patients with massive intraventricular hemorrhage (“packed ventricles”) and obstructive hydrocephalus that fails to improve rapidly with ventriculostomy portends extremely poor outcome. In patients with subarachnoid or intraparenchymal hemorrhage, moderate to large amounts of intraventricular blood are strong predictors of lethality.⁶¹ However, patients with spontaneous intraventricular hemorrhage appear to tolerate even large amounts of ventricular blood much better; they exhibit considerably less tendency to develop impaired consciousness or hydrocephalus and often retain full neurological capacities.^60,61 To our knowledge, the reason for this prognostic divergence is unclear at present.

Intraventricular hemorrhage is a poor prognostic factor in patients with IPH;^4,62 larger volume and early growth of intraventricular clot are predictive of mortality and unfavorable functional outcome.^22,63 External ventricular drainage catheters are inserted to treat the resulting hydrocephalus, but all too often drainage is insufficient because of obstruction of the catheter by the clotted blood. Furthermore, drainage through ventriculostomy has never been shown to accelerate the clearance of intraventricular blood. Intraventricular infusion of thrombolytics aimed at hastening this clearance is currently being tested with promising initial results.⁶⁴

MICROHEMORRHAGES

Susceptibility-weighted MR sequences, particularly T2^*-weighted GRE, enable us to recognize asymptomatic microscopic hemorrhages with enormous accuracy (Figures 10-30 and 10-31). Microhemorrhages are seen as small areas of signal loss due to the magnetic susceptibility effect caused by deposits of hemosiderin.⁶⁵ These lesions have become the focus of extensive research, and knowledge about their significance and implications is growing rapidly. The current status of such knowledge can be briefly summarized as follows:

Figure 10-30 A 55-year-old man with history of uncontrolled hypertension presented with right-sided hemiparesis. Computed tomography scan of the brain (left) showed a left posterolateral putaminal hemorrhage. Gradient-recall echo sequence of his magnetic resonance imaging (right) revealed multiple additional microhemorrhages involving the deep subcortical regions, specifically the right putamen and bilateral thalami (arrows).

Figure 10-31 A 56-year-old woman with history of refractory hypertension developed sudden right-sided hemisensory loss. Computed tomography scan (left) showed a left thalamic hemorrhage. On a previous admission for hypertensive encephalopathy, the gradient-recall echo sequence of the magnetic resonance imaging (right) had demonstrated the presence of a left thalamic microhemorrhage (black arrow) at the same site of the subsequent hematoma.