Вы находитесь на странице: 1из 17

Thalamic hemorrhage

By Julien Bogousslavsky MD (Dr. Bogousslavsky of Genolier Swiss Medical Network has no relevant financial relationships to disclose.)
Jorge Moncayo-Gaete MD (Dr. Moncayo-Gaete of the International University of Ecuador has no relevant financial relationships to disclose.)
Originally released February 28, 1995; last updated July 21, 2016; expires July 21, 2019


This article includes discussion of thalamic hemorrhage, posterolateral hematomas, dorsal hematomas, posterior-
dorsal hematomas, medial hematomas, and anterolateral hematomas. The foregoing terms may include synonyms,
similar disorders, variations in usage, and abbreviations.


The thalamus is involved in about 1 of every 6 nontraumatic intracerebral hemorrhages. Hemisensory loss, decreased
level of consciousness, and hemiparesis are the usual manifestations of thalamic hemorrhage; nevertheless,
depending on hematoma size and selective or global involvement of the different thalamic nuclei and neighboring
structures, virtually any clinical neurologic finding may be seen in the setting of thalamic hemorrhages. In this article,
the author thoroughly address the broad clinical spectrum in terms of the intrathalamic location of both large and
small bleedings. They also summarize the epidemiology, etiology, diagnostic workup, prognosis, and latest medical
and surgical treatment options for thalamic hemorrhages.

Key points
• Thalamic hemorrhage is the second most common location of intracerebral hemorrhage,
accounting for 10% to 15% of all hemorrhages.
• The clinical picture depends entirely on hematoma size, selective or global involvement of
the different thalamic nuclei, and the involvement of neighboring structures.
• Arterial hypertension is the most common etiology, regardless of topographic location and
hematoma size.
• Treatment is, for the most part, supportive medical care, including timely blood-pressure

Historical note and terminology

During the early decades of the twentieth century, French neurologists (particularly Dejerine, Foix, and their
colleagues) made important contributions concerning the vascular anatomy and pathology of the thalamus, including
the description of clinical manifestations resulting from lesions at different vascular territories (Dejerine and Roussy
1906; Foix and Hillemand 1925). At the time, the so-called “thalamic vascular syndrome” was defined as a persistent
contralateral hemianesthesia affecting both superficial and deep sensory modalities, a transient mild hemiparesis, and
hemiataxia, with possible subsequent development of intolerable pain and choreoathetotic movements in the affected
limbs (Dejerine and Roussy 1906). Some years after the initial description of the thalamic syndrome, Lhermitte and
Baudouin provided some clinical findings that helped to discriminate between ischemic and hemorrhagic lesions of the
thalamus (Lhermitte 1925).

Traditionally, thalamic hemorrhages, along with those located in the caudate and putamen, were considered to be
basal ganglionic hemorrhages. In 1959, however, CM Fisher pointed out abnormalities of pupillary and oculomotor
function observed in 13 patients with thalamic hemorrhages out of 102 patients with pathologically confirmed
intracerebral hemorrhage. Fisher also found greater sensory deficit than motor dysfunction, as well as speech or
behavioral manifestations resulting from the involvement of the left or right thalamus, respectively (Fisher 1959).

The introduction of the CT scan 40 years ago and, more recently, of brain MRI technology has made it possible to
identify small hematomas, describe clinical subtypes of thalamic hemorrhages, and improve insight into the function of
the different thalamic nuclear regions.

Clinical manifestations

Presentation and course

Thalamic hematoma characteristically occurs during activity; onset during sleep or rest is unusual (Steinke et al 1992;
Kumral et al 1995). Once the neurologic symptoms begin, they most often progress gradually over a period of minutes
or, less often, hours (Kumral et al 1995). Transient clinical signs resembling transient ischemic attacks may occur,
though not commonly, in intracerebral hemorrhages. Thus, in a cohort of 17 patients with intraparenchymal
hematomas and transient signs, 2 patients (both over 60 years of age) had small spontaneous thalamic hematomas
(7.7 ml and 21 ml) with mild neurologic deficits (respective NIHSS scores 2 and 3) lasting 30 minutes and 5 hours,
respectively (Kumar et al 2016).

Clinical manifestations of thalamic hemorrhages are broad. Their occurrence depends entirely on hematoma size,
selective or global involvement of the different thalamic nuclei, and the involvement of neighboring structures.
Hematomas have been classified based on topographical locations, size, and vascular territories (Hirose et al 1985;
Kawahara et al 1986; Steinke et al 1992; Chung et al 1996).

Posterolateral hematomas. Fifty percent of all thalamic hematomas are located in the posterolateral region
(Kawahara et al 1986; Kumral et al 1995; Chung et al 1996). Sensory disturbances are commonly seen in large and
small posterolateral hematomas, due to the involvement of both the ventral posteromedial and the ventral
posterolateral nuclei. Pure sensory stroke suggestive of, but not specific for, thalamic stroke has been observed
occasionally in posterolateral thalamic hemorrhage (Paciarioni and Bogousslavsky 1998). Spinothalamic, lemniscal,
and discriminative modalities of sensation can be affected in different patterns. The distribution of sensory loss is
variable, although hemibody hypesthesia is often found (Hirose et al 1985). In some very rare cases, acute isolated
numbness restricted to the contralateral tip of the tongue and the lower lip may result from a small thalamic
hematoma involving the medial part of the posterior ventromedial thalamic nucleus (Shimohata et al 2014). Large and
small hemorrhages may involve the adjacent posterior limb of the internal capsule, resulting in sensory loss associated
with variable degrees of contralateral hemiparesis (Kumral et al 1995). Sensory ataxic hemiparesis may also occur but
has been seen less often. The level of consciousness depends on hematoma size; stupor or coma occurs with large
hematomas, whereas alertness is preserved with small hematomas (Chung et al 1996).

An extensive spectrum of oculomotor disturbances is associated more frequently with large posterolateral hematomas.
The most common abnormalities include horizontal-gaze deviation toward the lesion, upward gaze palsy, combined
upgaze and downgaze palsy, and skew ocular deviation (Hirose et al 1985; Kawahara et al 1986). Contralateral gaze
preference, ipsilateral Horner syndrome, horizontal gaze palsy, and convergence spasm (peering at the tip of the nose)
may also occur, although less often (Kawahara et al 1986; Kumral et al 1995; Chung et al 1996). Interruption of
corticofugal fibers mediating saccadic and smooth-pursuit eye movements at the level of posterior thalamus is thought
to be responsible for hypometric saccades away from the hematoma, ipsilateral defective smooth-pursuit movements,
and ipsilateral-reduced optokinetic nystagmus (Hirose et al 1985). Hemianopia and quadrantanopia are rare (Hirose et
al 1985; Kumral et al 1995). Aphasia (global, transcortical, or Broca type) or mutism in dominant hemisphere lesions,
hemineglect, poor drawing, and poor copying in right-side thalamic bleeding are not frequent, although when present,
they are mostly related with large hematomas (Hirose et al 1985; Kawahara et al 1986; Kumral et al 1995; Chung et al
1996). Though a rather uncommon occurrence, agraphia may be the noticeable clinical finding in left-sided
posterolateral hematomas, most likely due to the disruption of both thalamocortical and cortico-thalamocortical loops
caused by reduced blood flow in the left cerebral cortex and thalamus as a result of the bleeding (Osawa et al 2013).

Involuntary movements may be seen, including myoclonus, asterixis, dystonia, chorea, and tremor. These may occur
in isolation or, more often, in a mixed pattern, anywhere from weeks to years after posterolateral hemorrhage (Kim
2001). Damage of the ventroposterior lateral and ventroposterior medial nuclei and, to a lesser extent, of the posterior
limb of the internal capsule is the anatomical basis of these involuntary movements (Kim 2001).

Pusher syndrome (contraversive pushing away from nonparetic side, leading to a loss of postural balance) occurs in
approximately one third of thalamic strokes and has often been associated with large posterior hematomas (Karnath et
al 2005). The posterior thalamus seems to influence pathways for sensing gravity orientation.

Dorsal hematomas. The frequency of dorsal hematomas is variable. A low frequency of 8% was found in a series of
small hematomas (less than 2 cm in mean diameter), whereas series including both small and large dorsal hematomas
have reported a frequency ranging between 15% and 28% (Kawahara et al 1986; Kumral et al 1995; Chung et al
1996). Consciousness is usually preserved. Ocular abnormalities are often absent; but when present, Horner syndrome
and upward gaze palsy have frequently been noticed. Large left-side hematomas may produce aphasia (global or
transcortical type), whereas corresponding right-side lesions have been associated with contralateral anosognosia
(Kumral et al 1995). Mild or moderate contralateral hemiparesis may occur due to extension of bleeding over the
corona radiata. Sometimes, the only clinical finding is pure motor stroke or sensorimotor deficit. In either case, the
disorder may be confused with a lacunar infarct. Inability to stand (thalamic astasia) despite normal motor power and
alertness is found in only a few cases, with improvement occurring between 1 week and 5 weeks after appearance
(Masdeu and Gorelick 1988).

Posterior-dorsal hematomas. Small hemorrhages may be confined to the far posterior area of the thalamus
(posterior-dorsal hematomas), although they are rarely observed. As with dorsal hematomas, consciousness usually
remains unaffected. Sensory and motor deficits are often transient and minimal or absent altogether. The pulvinar
nucleus and the medial geniculate body are often affected. Therefore, transient constructional apraxia, topographic
memory disturbance, and contralesional auditive extinction have been found in nondominant lesions, whereas left-side
hematomas may be associated with fluent aphasia (Kawahara et al 1986). A small hemorrhage involving the lateral
geniculate body produced a transient horizontal nystagmus (spontaneous and evoked gaze) and a contralateral
homonymous hemianopia (Han et al 2009).

Medial hematomas. Medial hematomas make up for one sixth of all thalamic hemorrhages (Kumral et al 1995;
Chung et al 1996; Tokgoz et al 2013). Early in the course, oculomotor abnormalities such as paresis of the vertical
gaze, Horner syndrome, and conjugate-gaze deviation opposite to the hematoma (the so-called “wrong way eyes”) are
common in large hematomas, although not in small ones (Kumral et al 1995; Chung et al 1996). Motor and sensory
deficits are mild and often transient in small hematomas restricted to the medial thalamus. Disturbances of
consciousness are often seen in medial hematomas and may fluctuate from confusion to stupor, depending on
hematoma size. These hematomas nearly always involve the intralaminar nuclei (central lateral, paracentral, and
centromedian), thus, hindering projections to the midbrain reticular formation. Moreover, large medial hematomas
spread to the midbrain, also contributing to impairment of awake state (Chung et al 1996). In some instances, onset of
hematoma with headache, vomiting, nuchal rigidity, and impairment of consciousness due to ventricular drainage into
the third ventricle may be confused with a subarachnoid hemorrhage. Later in the course, amnesic syndrome,
personality changes, and abulia may be the notable complaints, a result of damage to the medial thalamus'
connections to the limbic system and prefrontal cortex (Kawahara et al 1986).

Anterolateral hematomas. Rates of anterolateral hemorrhage vary between 5% and 20% (Kawahara et al 1986;
Kumral et al 1995; Chung et al 1996). Ophthalmological examination is usually unremarkable in small hemorrhages,
whereas large ones impair vertical gaze (Kumral et al 1995). Hemiparesis occurrence is related to involvement of the
anterior portion of the posterior limb of the internal capsule. Sensory deficits are mild and transient. Confusion in the
acute stage is often observed, and verbal-memory deficit, inattention, apathy, and abulia may be early and long-
lasting prominent clinical findings (Kawahara et al 1986; Chung et al 1996). These symptoms are due to the damage of
nuclear structures projecting to the frontal lobe. In dominant-side lesions, mutism and aphasia (global or transcortical)
are less often reported, as are neglect, anosognosia, and visual and tactile extinction in right-side hematomas (Kumral
et al 1995).

Global or large hematomas. Finally, approximately 10% to 18% of all thalamic hematomas are of the global type
(Chung et al 1996; Tokgoz et al 2013). Most commonly observed are nonspecific symptoms such as headache,
vomiting, and a decreased level of consciousness at presentation, results of increased intracranial pressure and
involvement of the brainstem reticular activating system. Ophthalmological examination may reveal a loss of upward
gaze and, less frequently, combined upgaze and downgaze paresis, pure downgaze paresis, and skew deviation.
Horizontal gaze preference toward the hematoma and, more rarely, “wrong way eyes,” has also been noticed (Messe
and Cucchiara 2003). Usually, both pupils are miotic and react poorly to light; this is due to involvement of the rostral
sympathetic pathway and damage to the pupillary reflex arc running to the third nerve nuclei in the midbrain. At
times, the ipsilateral miotic pupil is smaller than its counterpart. Selective miosis in the side of hematoma may occur,
although rarely. Retractory nystagmus and convergence disorders may also be found when hematomas spill out to the
thalamus, affecting the midbrain. Severe contralateral sensory and motor deficits are nearly always seen (Chung et al
1996). Language disorders and hemineglect may occur as well (Steinke et al 1992).

Prognosis and complications

The literature shows that approximately 9% to 32% of patients with thalamic hematoma die (Kumral et al 1995; Chung
et al 1996; Inagawa et al 2003; Shah et al 2005; Tokgoz et al 2013). The highest mortality rates have occurred in
patients with global (82%) and medial (61%) thalamic hemorrhages, whereas the lowest (6%) has been observed in
patients with posterolateral hematomas (Tokgoz et al 2013).

In general, outcome is associated with hemorrhage size (Kumral et al 1995). This is true whether hemorrhage size is
estimated by CT (67% mortality for hemorrhages greater than 10 cm3 in volume vs. 8% for those less than 10 cm3) or
by clinical signs (Kwak et al 1983). In particular, the level of consciousness on admission is predictive of outcome: 60%
of patients who are stuporous or comatose on admission die; this is compared to only 7% of those who are alert or
drowsy (Steinke et al 1992). Moreover, poor outcome 3 months after thalamic hemorrhage has been found to be
related to stroke severity, as per the Canadian Neurological Scale (Shah et al 2005). Early hematoma growth has been
considered a marker of poor prognosis. In fact, significant hematoma expansion has been observed to occur in
approximately 30% of patients with spontaneous intracerebral hematoma in the first 24 hours after onset. For each
10% hematoma enlargement, a consequent 5% increase in hazard of death and a 15% increase in poor functional
outcome were noted in a pooled meta-analysis of 218 patients with spontaneous intracerebral hemorrhage (Davis et al

In a retrospective series of 101 patients with thalamic hemorrhages, ventricular drainage occurred more often in
global (94%) and medial (61%) bleedings and less frequently in anterolateral hematomas (Tokgoz et al 2013).
Although controversial, the bulk of evidence suggests that intraventricular extension does seem to be associated with
higher mortality (Steinke et al 1992; Kumral et al 1995). The mechanism by which intraventricular extension exerts its
negative effect is not clear. Although intraventricular hemorrhage is associated with increased size and with
hydrocephalus, both of which are poor prognostic signs, intraventricular extension is an independent risk factor for
death (Young et al 1990).

Dysphagia is not uncommon in patients with acute thalamic hemorrhage. In 113 patients (mean age of 68) with acute
thalamic hemorrhage, a bedside swallowing assessment (repetitive saliva swallowing test and modified water
swallowing test) was carried out 2 days after hemorrhage onset. The hematoma was restricted to the thalamus in only
16% of these patients, whereas it also involved the adjacent internal capsule (70%) or the midbrain (14%) in the rest
of the patients. At initial evaluation, 55% of the 113 patients had dysphagia; compared to patients without swallowing
abnormalities, these patients were older, and they had a large median volume of hematoma, more intraventricular
extension, a lower mean Canadian Neurological Scale score, more aphasia and neglect, a longer length of stay, and a
lower rate of oral intake at hospital discharge (Maeshima et al 2014).

Functional recovery in smaller hemorrhages depends on the site as well as the size of hemorrhage (Kwak et al 1983).
In recovery of activities of daily living, dorsal and anterolateral hemorrhages have the best prognosis, whereas more
than one third of patients with posterolateral hemorrhages remain dependent (Chung et al 1996). Medial hemorrhages
also render a small percentage of patients dependent because of behavioral and cognitive deficits (Kawahara et al

Hydrocephalus is not an infrequent complication of thalamic hemorrhage, occurring in about 30%. In most cases, it is
probably due to the presence of subarachnoid blood impairing cerebrospinal fluid resorption.

Hypertensive thalamic hemorrhage has been thought to occur once in a lifetime. Repeated ipsilateral or contralateral
hypertensive thalamic hemorrhage is uncommon; rebleeding may occur with an interval of months to years after the
initial thalamic event. Primary hemorrhages that occur simultaneously in both thalami are uncommon. In a series of
105 patients (mostly from Asian background) with primary multiple simultaneous intracerebral hemorrhages identified
in the literature from 1950 to 2013, 18% to 19% of patients with an average age of 64, of which 13 were male, had
hemorrhages simultaneously in both thalami. The mortality rate in these patients was 31% (6 patients), whereas 47%
(9 patients) had a poor functional prognosis, and only 21% (4 patients) had a favorable outcome (Laiwattana et al

The thalamic pain syndrome of troubling dysesthesias and spontaneous pain over the contralateral side occurs after a
latency of days to weeks after the initial ictus and is often resistant to analgesics. It complicates thalamic hemorrhage
less frequently (less than 20%) than infarction, suggesting that a specific, partial destruction of the posterior lateral
region is required for its genesis (Kawahara et al 1986).

Acquired complex multimodal perceptual (sound-color, grapheme-taste, and sound-tactile) synesthesias (the confusion
of different sensory modalities) were reported in a 45-year-old hypertensive patient 9 months after a thalamic
hematoma involving the pulvinar, lateral posterior, and ventral posterior lateral nuclei of the thalamus (Fornazzari et al
2012). Two hypotheses have been proposed to explain this exceedingly rare complication after a thalamic hematoma:
an anomalous cortical connection or an aberrant activation of anomalous sensory regions in response to stimulation.

Clinical vignette

Vignette 1. On awakening, a 51-year-old right-handed Hispanic man suddenly experienced severe headache and
numbness on the left facial side, followed several minutes later by numbness in the left arm and left leg. Afterwards,
he was unable to walk without assistance. The patient's medical history included untreated arterial hypertension 3
months prior to this admission and cigarette use (around 10 cigarettes per day) over 30 years. He denied alcohol or
substance abuse. His bed partner complained of his loud nocturnal snoring, but no apneas or excessive daytime
sleepiness had been previously observed.

On examination, the patient's body mass index was 31.24 kg/m2, and his blood pressure was 180/100 mmHg. No
cardiac murmurs were audible, and he was drowsy. Both eyes showed downward deviation, with additional inward
deviation of the right eye.{embed="pagecomponents/media_embed" entry_id="10137"} An upward gaze palsy on
voluntary saccadic and pursuit eye movements was observed. The pupils were equal in size (1.5 mm in diameter) and
poorly reactive to light. Convergence was also impaired. There was no neglect and hemianopia by confrontation. A left
sensory loss involving light touch, pain, temperature, position, and vibration was found. A left flaccid hemiparesis
involving the arm and leg was also noticed. Kernig and Brudzinski signs were present.

Blood cell count, routine serum chemistries (including lipid profile), and electrolytes were normal. Prothrombin time
(PT), activated partial thromboplastin time (APTT), and fibrinogen and platelet count were also normal. An
electrocardiogram and a transthoracic echocardiogram were normal. A nonenhanced CT of the patient's brain showed
a large, right thalamic hemorrhage extending into the posterior limb of the internal capsule, putamen, and upper
midbrain.{embed="pagecomponents/media_embed" entry_id="10138"} Thalamic bleeding was associated with
hydrocephalus, and the blood extended to the third ventricle and the lateral ventricles' occipital horns.

The patient received only supportive care. An angiotensin-converting enzyme inhibitor was introduced on the fourth
day after onset of symptoms.

Vignette 2. While doing housework, a 30-year-old, right-handed Hispanic woman suddenly developed an acute
throbbing pain in the frontal right side that radiated to the ipsilateral occipital region. Approximately 5 minutes later,
she experienced paresthesias in the distal part of her left arm and then in the left leg. She had been healthy, although
slightly overweight (BMI 26.56 kg/m2). She was free of any significant medical history and did not take any medication
or use tobacco, alcohol, or illicit drugs. On arrival in the emergency room, her blood pressure was 110/60 mm Hg and
cardiac rhythm was regular; she was fully consciousness, and no speech disturbances were noted. A slight upward
paresis and a right Horner syndrome were found. Visual fields and convergence were normal. Perception of pinprick,
light touch, vibration, and position sense were decreased over the left hemibody, and hemiataxia involving mainly the
left upper limb was also seen. No motor deficit was noted. On the third hospital day, she complained of symptoms
suggestive of binge eating disorder, which eventually subsided one week later.

Blood cell count, routine serum chemistry, coagulation screening, and a transthoracic echocardiography were all
normal. No toxicology screen was done. An acute right anterior thalamic hemorrhage extending to the right upper
midbrain was found on CT scan and brain MRI.{embed="pagecomponents/media_embed" entry_id="10139"} On the
second hospital day, a digital subtraction angiography of the posterior circulation did not reveal any
abnormality.{embed="pagecomponents/media_embed" entry_id="10140"} A second brain MRI performed 4 months
after the acute thalamic hemorrhage disclosed a cavernous malformation in the right midbrain peduncle extending to
the ipsilateral thalamus.{embed="pagecomponents/media_embed" entry_id="10141"}

Biological basis

Etiology and pathogenesis

The most common underlying etiology, regardless of topographic location and hematoma size, is longstanding arterial
hypertension, as may be seen in more than 80% of patients (Steinke et al 1992; Kumral et al 1995; Chung et al 1996).
Although rare, acute rises in blood pressure have also been documented in certain instances of thalamic hemorrhage,
such as in autonomic dysreflexia (uncontrolled sympathetic output in patients with a chronic spinal cord injury above
the T6 spinal level) (Eker et al 2014).
Arteriovenous malformations involving the thalamus account for 11% of all arteriovenous malformations and
approximately half of the deep arteriovenous malformations (Stefani et al 2002). These deep lesions with central
drainage into either the basal vein of Rosenthal or the internal cerebral vein are more prone to bleeding (Sasaki et al
1998). Thus, thalamic hemorrhage may occur as the initial clinical presentation of arteriovenous malformations or
rebleeding (Sasaki et al 1998). Intraparenchymal hemorrhage is the second most common clinical presentation of
cavernous malformations. Thalamic cavernous angiomas are not common and are seldom found as etiology.

Intracranial hemorrhage is a well-established major complication of anticoagulant and fibrinolytic agents. Warfarin-
associated thalamic hemorrhage, however, is not commonly found as etiology. Bleeding may occur either with high
levels of anticoagulation or when the international normalized ratio is within the therapeutic range (Steinke et al
1992). Large, deep hemispheric hematomas also involving the thalamus have been found in cases of intraarterial
thrombolysis (Kase et al 2001). A type 1 heterozygous protein C deficiency was complicated with a left thalamic
hematoma without associated cerebral venous thrombosis or venous hemorrhagic infarction (Matsuyama et al 2002).

Hematoma in the thalamus subsequent to rupture of an aneurysm arising from P1 segment of the posterior cerebral
artery has been reported. In this instance, a CT scan taken 48 hours after bleeding showed a thalamic hematoma and
a rapid disappearance of blood in the subarachnoid space. Brain MRI demonstrated a close relation between the
thalamic hematoma and the dome of the aneurysm (Crum and Wijdicks 2000). Another case of thalamic hemorrhage,
involving the pulvinar and initially thought to be due to chronic arterial hypertension, was found on further imaging a
month later to be the result of a lateral posterior choroidal aneurysm, which was successfully treated by surgical
resection (Fukuda et al 2013).

Thalamic hemorrhage is an uncommon complication after internal carotid endarterectomy or stenting (Chamorro et al
2000). In rare cases, thalamic hemorrhage may be a complication of stereotactic removal of intraventricular tumors
(Morita and Kelly 1993), or it may be the initial presentation of a previously unknown anaplastic astrocytoma (Li et al
2013). Stereotactic thalamotomy for movement disorders can be followed by perioperative small thalamic hematomas
(Terao et al 2003); more rarely, delayed thalamic hemorrhage has been reported after deep-brain stimulation
(Zesiewicz et al 2008).

Other less common etiologies include polyarteritis nodosa (De Reuck 2003), pseudoxanthoma elasticum as a first
manifestation (Bock and Schwegler 2008), Sturge-Weber syndrome (Nakajima et al 2014), chronic alcoholism (Chung
et al 1996), drug abuse (including cocaine, amphetamines and sympathomimetics) (Cantu et al 2003), preeclampsia
(Skidmore et al 2001), multiple honeybee stings (Remes-Troche et al 2003), and Plasmodium vivax malaria in the
absence of thrombocytopenia and disseminated intravascular coagulation (Sarkar et al 2012). Although uncommon,
single or recurrent thalamic hematomas may also occur (with or without concomitant intraventricular hemorrhages) in
the setting of moyamoya disease, particularly among young Asian and non-Caucasian adults (Saeki et al 1997).

A patient with a history of untreated mild arterial hypertension was reported to have developed a thalamic hematoma
1 hour after taking a single dose of 50 mg of sildenafil for the first time in his life. In this report, it was suggested that
sildenafil might have caused cerebral vasodilation, leading to an increase of blood flow in the brain and raising the risk
of intracranial bleeding (Alpsan et al 2008). Despite laboratory and neuroimaging investigations, an etiology cannot be
identified in 10% to 30% of patients with thalamic hemorrhage (Chung et al 1996).

Each thalamus is a 4 cm oval-shaped structure that lies adjacent to the third ventricle. It is comprised mainly of gray
matter and serves as a relay station for most central neural systems, each compartmentalized into a nerve nucleus.
There are 4 important sources of blood supply for the thalamus: the thalamoperforants, which arise from the basilar
artery bifurcation and supply the medial aspect of the thalamus; the thalamogeniculates, which supply the
posterolateral aspect; the posterior choroidal artery, which supplies the dorsal portion; and the tuberothalamic artery,
which arises from the posterior communicating artery and supplies the anterior portion. The compartmentalization of
neurons into nuclei gives rise to different clinical syndromes when different regions of the thalamus, supplied by
different arterial systems, are affected.

Surges in arterial pressure, weakened vessel wall structure, and impaired hemostasis contribute to arterial or venous
rupture and subsequent hemorrhage. Of these, vascular structural pathology appears to be most important.
Hypertensive vasculopathy, the most frequent cause of thalamic hemorrhage, is a degenerative change in the wall of
small arteries characterized by loss of muscular components, hyaline and fibrinoid change, and microaneurysm
formation (Fisher 1971). As the thalamus is supplied almost exclusively by these small arteries, it is especially
vulnerable to the pathologic consequences of hypertensive vasculopathy, including hemorrhage. Other causes of
weakened arterial wall structure include arteriovenous malformations in which high venous pressure and congenitally
abnormal vessel wall structure lead to an increased risk of cerebral hemorrhage. Sympathomimetic drugs,
amphetamines, and cocaine can produce intracerebral bleeding by inducing vasculitis-like abnormalities or the rupture
of previously occult arteriovenous malformation, or it can be associated with hypertensive crisis (Cantu et al 2003).
Abnormal vessel wall structure in the neovascularity of cerebral neoplasms leads to their propensity to hemorrhage
(Hirano and Matsui 1975).

Active bleeding usually is completed within 20 hours after onset. Blood infiltrates along white matter tracts and
compresses the gray matter, producing an area of hypoperfusion surrounding the hematoma, which may represent
either a true perihemorrhagic ischemia or a zone of reactive oligemia due to a reduced metabolic demand (Schellinger
et al 2003). Because of its close proximity to the third ventricle, intraventricular extension is common in thalamic
hemorrhage, occurring in 30% to 60% of patients (Steinke et al 1992; Kumral et al 1995). Brain edema after
intracerebral hemorrhage first appears in 7 to 8 hours and progresses over the next 1 to 5 days. Interaction between
thrombin and vascular endothelial growth factor, which results in altered vascular permeability, is thought to be the
key step in brain edema development. Resorption of blood takes place over weeks to months, leaving a cavity lined by
hemosiderin laden macrophages and surrounded by ischemic necrotic tissue.


Thalamic hemorrhages make up 10% to 15% of all intracerebral hemorrhages. However, clinical series of thalamic
hemorrhages based on Turkish and Japanese populations have showed higher figures (Kumral et al 1995; Inagawa et
al 2003). Thalamic hemorrhages occur more frequently in people 60 years of age and older (Hirose et al 1985;
Kawahara et al 1986; Steinke et al 1992; Chung et al 1996; Shah et al 2005). Most CT-based series of thalamic
hemorrhages are small, which has hindered establishing clear gender predominance. However, females prevailed in 2
clinical series of thalamic hemorrhages (Kumral et al 1995; Chung et al 1996). Restricted thalamic hemorrhages
occurred more frequently than thalamic infarcts in nonwhites (Steinke et al 1992).


Age, male sex, and arterial hypertension are well-established risk factors for intracerebral hemorrhage (Ariesen et al
2003). Available evidence suggests that blood pressure lowering strategies reduce the risk of a first stroke by 25% to
30% (Dahlof et al 2002). Intracerebral hemorrhage has an annual recurrent bleeding rate of approximately 2% (Hill et
al 2000). Besides benefits in primary prevention, reduction in blood pressure reduces the risk of further intracerebral
bleeding by 50% in patients with prior hemorrhage (PROGRESS Collaborative Group 2001). In case-control studies,
high alcohol intake (greater than 56 g/d) has been found to lead to a 3-fold increase in the risk of intracerebral
hemorrhage by impairing coagulation and directly affecting the integrity of cerebral vessels (Ariesen et al 2003). Thus,
there is no doubt that an efficient reduction in blood pressure and ending of alcohol abuse are important measures for
the primary and secondary prevention of hemorrhage in the thalamus. The current Guidelines of the American Heart
Association recommend after the acute period a goal blood-pressure lower than 130/80 mm Hg (Hemphill et al 2015).
The association of smoking and intracerebral hemorrhage is still controversial; however, it is altogether advisable that
current smokers quit smoking (Ariesen et al 2003).

Although coagulopathy may also be a risk factor for thalamic hemorrhage, it is difficult to translate this into a strategy
for primary prevention of thalamic hemorrhage.

Other underlying conditions (such as arteriovenous malformations) leading to or increasing risk of thalamic
hemorrhage are often unknown prior to the intracerebral hemorrhage. This makes preventative strategies difficult in
these patients as well. After hemorrhage has occurred, obliteration of arteriovenous malformations by a single or
combined treatment modality (microsurgery, endovascular embolization, or stereotactic radiosurgery) may be
undertaken to prevent subsequent hemorrhages, primarily when the treatment modality warrants both low
complication and higher obliteration rates, as in the case of 48 patients with small arteriovenous malformations in the
thalamus who were treated by stereotactic radiosurgery (Koga et al 2010).

A protective effect of statins has been suggested based on lower neurologic deficits at admission, lower mortality, and
better outcome at discharge observed in 89 patients who had previously been receiving statin therapy in a cohort of
312 intracerebral hemorrhage patients (Leker et al 2009). Likewise, a meta-analysis (data mostly from observational
studies) showed that 698 patients with intracerebral hemorrhage who were previously on statins had better functional
outcomes and reduced mortality at 90 days compared with 1823 patients with intracerebral hemorrhage and no prior
statin therapy (Biffi et al 2011).

Differential diagnosis

A patient presenting with acute neurologic deficit related to thalamic function may have a cerebral infarction or
hemorrhage. There are no reliable clinical means of distinguishing the two, necessitating a diagnostic imaging study.

Diagnostic workup

Evaluation of a patient with thalamic hemorrhage should include a detailed history and physical examination to
identify possible risk factors or etiologies such as previous diagnoses of arterial hypertension or arteriovenous
malformation, use of anticoagulants, illicit-drug abuse, or abuse of alcohol.

Baseline laboratory studies should include complete blood and platelet counts, prothrombin time, partial
thromboplastin time, liver functions, renal panel, serum glucose, electrocardiogram, and chest x-ray. In adolescent or
young patients without risk factors for intracerebral hemorrhage, a toxicology screening should usually be carried out
(Hemphill et al 2015).

Due to its high sensitivity, specificity, rapid acquisition time, and availability at emergency departments, noncontrast
CT scan is still the preferred imaging procedure to exclude the presence of intracerebral hemorrhage (Hemphill et al
2015). It also allows definition of size, location of the bleeding within the thalamus, and spreading into neighboring
structures (internal capsule, lentiform nucleus, subthalamus, midbrain and subcortical white matter). In addition,
presence of ventricular blood, occurrence of hydrocephalus, and surrounding edema may be recognized with CT scan.
Hematoma evolution may be also monitored by noncontrast brain CT.

Conventional MR images with T1- and T2-weighted sequences are not sensitive to blood in the hyperacute stage,
whereas gradient echo-MRI sequences are as accurate as CT for detection of hemorrhage during this period (Macellari
et al 2014). In a multicenter study of 62 patients with acute intracerebral hemorrhage, gradient echo-MRI was found to
be useful for diagnosis with a sensitivity of 100% within the first 6 hours after symptom onset (Fiebach et al 2004).
Nevertheless, its use may be limited due to lack of tolerability or the presence of a cardiac pacemaker, or it may be
altogether unavailable.

Determination of the cause of thalamic hemorrhage relies on patient age and prior history. When thalamic hemorrhage
occurs in a patient with known arterial hypertension, often no other cause is sought, whereas in normotensive patients
and, particularly, those younger than 45 years of age with thalamic hemorrhage, a digital subtraction angiography is
still the currently preferred practice, according to results reported by nearly 700 physicians involved in the care of
intracerebral hemorrhage patients in 3 European countries (Cordonnier et al 2010). If hemorrhage suggests an
underlying structural lesion, further investigations may include MRI, MR angiography/venography, CT
angiography/venography, or conventional angiography (Morgenstern et al 2010; Macellari et al 2014; Hemphill et al
2015). MRI has been found to be superior to CT in providing useful data to rule out the presence of underlying
arteriovenous malformations or tumors, although small arteriovenous malformations may be missed with this
technique, or the underlying structural lesion may be obscured by the acute hematoma (Macellari et al 2014). MR-echo
gradient sequences identify cavernous malformations better than MRI. MR angiography or CT angiography may also
reveal structural lesions. CT angiography may provide better vascularization detail than MR angiography.

Approximately one third of patients with intracerebral hemorrhage showed the “spot sign” –defined as at least one
focus of enhancement within the hematoma margin and without external vascular communication—on CT angiography
performed early after symptom onset. There is currently no consensus about the minimum Hounsfield unit density,
size, and morphological patterns of this radiological sign (Thompson et al 2009; Delgado Almandoz et al 2010; Evans
et al 2010; Hallevi et al 2010). This bright spot is found somewhat less frequently when the bleeding involves either
the basal ganglia or the thalamus (Evans et al 2010). Moreover, contrast extravasation (seen as pooling of contrast in
the hematoma area after postcontrast CT in the location of the CTA spot sign) was observed in approximately half of
the patients with a spot sign on CT angiography within the first 6 hours after intracerebral hemorrhage (Evans et al
2010; Hallevi et al 2010). Early hematoma expansion on subsequent imaging has been associated with spot positivity
and contrast extravasation (Hallevi et al 2010), whereas the presence of the spot sign increases the risk of in-hospital
mortality and poor functional outcome at 3 months (Delgado Almandoz et al 2010). Contrast extravasation was
observed on CT angiography in 20% of 139 patients with primary intracerebral hemorrhages mostly located in the
deep gray matter. This radiological finding was associated with an increased rate of early hematoma expansion and
was found to be an independent predictor of poor outcome and mortality at 3 months (Li et al 2011). A 9-point
prediction score for identifying intracerebral hemorrhage patients at risk of hematoma expansion has been developed
and independently validated (Brouwers et al 2014). In the development cohort of this prediction score, the
hemorrhage was located in the basal ganglia and thalamus in nearly half of the cohort's 817 patients; 40% of the
hemorrhages were lobar, whereas the remainder were found in the brainstem and cerebellum. The prediction score
included clinical and radiological parameters available on initial evaluation. A high risk of hematoma growth was
associated with a shorter time to initial brain CT (less than 6 hours), a large baseline hematoma volume (> 60 mL), the
presence of the CTA spot sign, and warfarin use (Brouwers et al 2014). A high score (4 to 9 points) was associated with
a 4.5-fold increased risk of hematoma expansion as compared to a low score (0-3 points). In a secondary analysis that
excluded patients with previous warfarin treatment, the prediction score was associated with a 3.2-fold greater
likelihood of hematoma growth (Brouwers et al 2014). A prediction score that reliably identifies patients at the highest
risk of hematoma expansion would be a useful tool for selecting those requiring more intensive care or tailored
treatment to prevent hematoma growth. Additionally, it would be valuable for appropriately selecting patients for
clinical trials designed to evaluate different treatment methods to prevent expansion and, consequently, improve

The “black hole” sign, another imaging marker that may be useful to predict early hematoma expansion, was found in
14.6% of 206 patients on nonenhanced CT scan within 6 hours after onset of spontaneous intracerebral hemorrhage,
mostly located in the basal ganglia and thalamus (Li et al 2016). The black hole sign was defined as a hypoattenuated
area (black hole) encapsulated within a hyperattenuating hematoma with a clearly defined border, which may suggest
bleeding of different age within the hematoma. In this cohort of patients, hematoma growth on nonenhanced CT scan
performed within 30 hours of baseline imaging was found to occur 5 times more frequently in patients with black hole
sign than in those with no black hole sign, 32% versus 6%, respectively (Li et al 2016).


The treatment of patients with thalamic hemorrhage is, for the most part, supportive medical care. Due to medical and
neurologic instability during the acute phase of intracerebral hemorrhage, it is advisable that management take place
either in an intensive care unit or a stroke unit. Basic measures include continuous cardiopulmonary monitoring,
airway protection in patients with suppressed level of consciousness, screening for dysphagia, strict glucose control,
prophylaxis against deep venous thrombosis, early mobilization, and rehabilitation. Moreover, intracranial and cerebral
perfusion pressure, hemodynamic function, and neurologic function should be continuously monitored (Hemphill et al

Treatment of sustained, severely elevated blood pressure is advisable to avoid recurrent or continued hemorrhage.
The current Guidelines of the American Heart Association recommend lowering systolic blood pressure to 140 mm Hg
in patients with systolic blood pressure between 150 and 220 mm Hg and no contraindications to acute blood pressure
treatment. This recommendation is safe and may be effective in improving the functional outcome (Hemphill et al
2015). More aggressive treatment--preferably with short-acting antihypertensive agents and frequent monitoring of
blood pressure in the first hours after hemorrhage onset--is recommended when systolic blood pressure is higher than
220 mm Hg (Hemphill et al 2015).

Two prospective trials reported the effect of intensive blood pressure lowering within the first 6 hours after onset of
supratentorial hemorrhage (Anderson et al 2008; Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH)
Investigators 2010). In both trials, intensive blood pressure lowering was found to be associated with a reduction in
hematoma growth at 24 hours that was not associated with a poor clinical outcome. Thus, a first attempt to explore a
blood-pressure target in 346 patients (most of Chinese origin) with acute intracerebral hemorrhage found that
achieved on-treatment systolic blood pressure of between 130 and 140 mm Hg (median of 135 mm Hg) throughout
the first 24 hours was associated with the greatest reduction of hematoma growth (Arima et al 2010).

In an international multicenter prospective study (INTERACT-2) of 2829 intracerebral hemorrhage patients with a mean
age of 63.5 years, the safety and effectiveness of early intensive blood pressure lowering was compared with standard
antihypertensive treatment based on currently recommended guidelines. The study randomly assigned 1399 patients
(median NIHSS score of 10 points, 84% with a deep intracerebral hematoma) to early intensive treatment to lower
their blood pressure (target systolic level of <140 mm Hg within 1 hour), whereas the remaining 1430 patients
(median NIHSS score of 11 points, 83% with a deep intracerebral hemorrhage) were assigned to guideline-
recommended treatment (target systolic level of <180 mm Hg) (Anderson et al 2013). In both groups, the choice of
intravenous antihypertensive agent (mostly alpha adrenergic antagonist) was left up to the treating physician, and the
median time from onset of hemorrhagic stroke to initiation of intravenous treatment was shorter in the intensive-
treatment group than in the standard-therapy group (4.0 hours vs. 4.5 hours). A significant difference in mean systolic
blood pressure was observed among both groups at 1 hour (150 mm Hg in the intensive-treatment group vs. 164 mm
Hg in the standard-treatment group). The mean hematoma volumes at baseline for the patients undergoing intensive
blood pressure lowering and those assigned to guideline-recommended treatment were 15.7 ml and 15.1 ml,
respectively, and an absolute difference of 1.4 ml between both groups was observed at 24 hours (18.2 ml in the
intensive-treatment control group and 20.6 ml in the standard-treatment group). At 90 days, a nonsignificantly higher
rate of poor outcomes (death or major disability) was observed in the standard-treatment group (56%) as compared to
the intensive-treatment group (52%), although an ordinal analysis of scores on the modified Rankin scale suggested
that intensive blood pressure treatment did in fact improve functional outcomes (Anderson et al 2013). No difference
was observed in the death rate from any cause in either group. Consequently, the real benefit in outcome of early
blood pressure management (including the choice of blood pressure-lowering agent) in patients with acute
intracerebral hemorrhage must be answered by further studies.

In the last few months, a meta-analysis of 4 randomized controlled trials (comprising of 3315 patients with a mean age
of 63.8 years) showed after 3 months that intensive blood pressure treatment in the acute phase of intracerebral
hemorrhage did not reduce the mortality rate compared to standard management based on current guidelines. In
contrast, a nonsignificant lower worse outcome (death or dependency) and a significant, although modest, reduction of
hematoma expansion at 24 hours was observed in patients with intensive blood pressure treatment compared to
standard management based on current guidelines (Tsivgoulis et al 2014).

Intensive blood pressure reduction in the hyperacute (1 to 24 hours) and acute (2 to 7 days) phases of intracerebral
hemorrhage showed a trend toward a favorable outcome, which was estimated by an ordinal analysis of the modified
Rankin scores. This open, randomized controlled trial at its end included 2794 patients (68% enrolled in China) with
spontaneous intracerebral hemorrhage (median volume of 10.2 ml; thalamic or basal ganglia location in 77% of
patients) who were randomized into 2 blood pressure treatment groups. The first group had a target level of systolic
blood pressure of less than 140 mm Hg to be reached within 1 hour after randomization and maintained for the next 7
days. In the second group, treatment was started when systolic blood pressure was over 180 mm Hg. In both groups,
the main intravenous antihypertensive agents were urapidil (an intravenous alpha-adrenergic antagonist), followed by
nicardipine or nimodipine (calcium-channel blockers). At 90 days, an overall relative risk reduction of 13% in poor
functional outcome favored intensive systolic blood pressure treatment. The lowest risk of functional disability was
observed when systolic blood pressure ranged between 130 and 139 mm Hg in the acute phase of intracerebral
hemorrhage (Arima et al 2015).

In the last few months, the results of a meta-analysis assessing the safety and efficacy of early lowering of blood
pressure in acute intracerebral hemorrhage as opposed to standard management have become available. In this meta-
analysis, 1,427 patients with acute intracerebral hemorrhage from 4 randomized trials were assigned either an
intensive blood pressure treatment (target systolic blood pressure 140 mm Hg or lower or mean arterial pressure lower
than 110 mm Hg) or a conservative treatment (target systolic blood pressure 180 mm Hg or lower or mean arterial
pressure lower than 130 mm Hg). No significant differences in the rate of serious adverse events and mortality rate at
3 months were observed between the two groups. A trend toward a favorable outcome at 90 days (modified Rankin
Score 2 or lower) was observed in the group of patients with intensive blood pressure treatment, as was a reduced
(but not significant) hematoma expansion at 24 hours (Pan et al 2015).

Elevated intracranial pressure may develop in patients with large thalamic hemorrhages. Head elevation and
avoidance of hyposmolar intravenous fluids are basic measures in all patients with large hemorrhages.
Hyperventilation to a PCO2 of 25 mm Hg decreases intracranial pressure by lowering cerebral blood flow.
Hyperosmolar diuretics such as mannitol and hypertonic saline solution can also be useful to decrease elevated
intracranial pressure.

Obstructive hydrocephalus may complicate thalamic hemorrhage when there is intraventricular extension. Although
ventriculostomy is generally recommended for this complication, it has not been shown to improve prognosis (Young
et al 1990; Chung et al 1996).

In general, thalamic hemorrhages have not been considered for surgical therapy because of their deep location in the
brain and the fear that surgery might cause additional neurologic deficits. In the STICH multicenter trial, 1033 patients
with spontaneous supratentorial intracerebral hemorrhage were randomized to the best conservative treatment or
early surgical removal of hematoma (less than 72 hours after stroke onset). Open craniotomy was chosen as the
surgical procedure by most neurosurgeons. In this trial, 284 and 300 patients with basal ganglia or thalamic
hemorrhages were allocated to early surgery or conservative treatment, respectively. In these deep-hemorrhage
patients, no differences in favorable outcome at 6 months were noted between the 2 treatments (Mendelow et al
2005). To date, there is no convincing evidence of benefit of surgical treatment of thalamic hematomas (Mendelow et
al 2005; Hemphill et al 2015).

The benefits of minimally invasive operative procedures (endoscopic hematoma aspiration and thrombolytic therapy
plus stereotactic hematoma drainage) in cases of spontaneous supratentorial hemorrhages are still being investigated
through randomized controlled trials (Samadani and Rohde 2009; Wang et al 2009).

One hundred and five patients with a first thalamic hematoma (10-35 ml of volume) were non-randomly divided into 2
groups: the first group (45 patients) was treated by aspiration (within 4 to 48 hours after the onset of bleeding; 10.4-
hour mean time to operation) and subsequent thrombolysis with urokinase, and the second group (60 patients)
received conservative treatment (Chen et al 2012). A significant difference in cumulative mortality rate (28% in the
conservative group versus 11% in the aspiration group) was observed at 30 days after hemorrhage. The NIHSS score
at 30 days after stroke onset was significantly lower in the aspiration group (14.2) than in the medically treated group
(16.5). Half of the patients in the aspiration group had a favorable outcome (Glasgow Outcome Scale > 3) at 90 days
after stroke onset versus one-third of patients in the conservative group, which is a significant difference. There was
no difference between the groups with regard to rate of complications (rebleeding, intracranial infection, and
pneumonia) (Chen et al 2012).

In a metaanalysis that included 11 studies (totaling 1717 patients with primary supratentorial hemorrhage, an average
age between 56 and 67 years, and a mean hematoma volume from 33 to 59 ml), all the patients received conservative
medical treatment for intracerebral hemorrhage. The aim of the study was to compare the efficacy of minimally
invasive surgery (stereotactic and/or neuroendoscopic hemorrhage evacuation) against either open surgery or medical
management alone (Ramanan and Shankar 2013). Patients who underwent minimally invasive surgery showed a
significant 36% reduction in the relative mortality risk, a nonsignificant 5% reduction in death or dependent survival,
and a nonsignificant 24% increase in independent survival (Ramanan and Shankar 2013). This metaanalysis, thus,
suggests that minimally invasive surgery (stereotactic, neuroendoscopic, or burr hole evacuation) may be an effective
step in the treatment of primary supratentorial hemorrhage, although important issues remain to be clarified, such as
which patients will benefit most from this kind of intervention and what risks are involved.

The value of ultra-early hemostatic therapy (recombinant-activated factor VII) remains in doubt because no benefit on
mortality or functional outcome was demonstrated in 840 patients with noncoagulopathic intracerebral hemorrhages
included in the largest phase III trial, despite the hemostatic effect observed (Mayer et al 2008). Nevertheless, in a
posthoc analysis of this phase III trial, a better outcome was observed among patients aged less than 70 years, with a
baseline hematoma volume of less than 60 mL, a baseline intraventricular hemorrhage volume of less than 5 mL, and
a time from onset to treatment of less than 150 minutes (Mayer et al 2009). The effect of the hemostatic agent
tranexamic acid on hematoma growth is currently being investigated in a multicenter, randomized, placebo-controlled
(two arm 1;1), double-blind phase 2 trial (The Spot Sign and Tranexamic Acid on Preventing ICH Growth – AUStralasia
Trial) (STOP-AUST) based on positive results observed in trauma patients and in an observational study of ethnic Asian
patients with acute intracerebral hemorrhage. One hundred patients with acute intracerebral hemorrhage and “spot
sign” evaluated on CTA (considered an imaging marker of ongoing bleed) will be randomized to receive tranexamic
acid (active treatment arm) or a placebo within 4.5 hours of intracerebral hemorrhage onset (Meretoja et al 2014). The
primary outcome will be intracerebral hemorrhage growth at 24 hours and the secondary outcome measures will
include absolute increase in hematoma volume, major thromboembolic events, and modified Rankin scale score at 90
days (Meretoja et al 2014).

Special considerations

Pregnancy may be a risk factor for thalamic hemorrhage for a number of reasons. First, hemodynamic changes in
pregnancy, including increased cardiac output, heart rate, and blood volume, are believed to increase the risk of
intracranial hemorrhage from arteriovenous malformations and intracranial aneurysms (Skidmore et al 2001). Certain
pregnancy-related conditions may increase the risk of intracerebral hemorrhage, including bleeding diatheses such as
idiopathic thrombocytopenic purpura and disseminated intravascular coagulation. Finally, pregnancy-induced
hypertension may lead to a hypertensive vasculopathy and intracerebral hemorrhage (Skidmore et al 2001).


Effects of anesthetic agents on cerebral blood flow, cerebral metabolism rate, and intracranial pressure should be
considered in the acute or subacute phase of intracerebral hemorrhage in order to avoid worsening of neurologic
status either by increase in intracranial hypertension or critical reduction of perihematoma cerebral blood flow.
Inhalational anesthetic agents produce direct cerebral vasodilatation and an increase in cerebral blood volume,
whereas hypnotic agents, benzodiazepines derivatives, and opioids reduce cerebral metabolic rate and cerebral blood

References cited

Alpsan MH, Bebek N, Ciftci FD, Coban O, Bahar S, Tuncay R. Intracerebral hemorrhage associated with sildenafil use: a
case report. J Neurol 2008;255:932-3. PMID 18465112

Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage.
New Engl J Med 2013;368(25):2355-65. PMID 23713578

Anderson CS, Huan Y, Wang J, for the INTERACT Investigators. Intensive blood pressure reduction in acute cerebral
haemorrhage trial (INTERACT): a randomised pilot trial. Lancet Neurology 2008;7:391-9. PMID 18396107

Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH) Investigators. Antihypertensive treatment of acute
cerebral hemorrhage. Crit Care Med 2010;38(2):637-48. PMID 19770736

Ariesen MJ, Claus SP, Rinkel GJ, Algra A. Risk factors for intracerebral hemorrhage in the general population: a
systematic review. Stroke 2003;34(8):2060-5. PMID 12843354

Arima H, Anderson CS, Wang J, for the Intensive Blood Pressure Reduction in Acute Cerebral Haemorrhage Trial
Investigators. Lower treatment blood pressure is associated with greatest reduction in hematoma growth after acute
intracerebral hemorrhage. Hypertension 2010;56:852-8. PMID 20823381

Arima H, Heeley E, Delcourt C, et al. Optimal achieved blood pressure in acute intracerebral hemorrhage INTERACT2.
Neurology 2015;84(5):464-71. PMID 25552575

Biffi A, Devan WJ, Anderson CD, et al. Statin use and outcome after intracerebral hemorrhage: case-control study and
meta-analysis. Neurology 2011;76:1581-6. PMID 21451150

Bock A, Schwegler G. Intracerebral haemorrhage as first manifestation of pseudoxanthoma elasticum. Clin Neurol
Neurosurg 2008;110:262-4. PMID 17964712

Brouwers HB, Chang Y, Falcone GJ, et al. Predicting hematoma expansion after primary intracerebral hemorrhage.
JAMA Neurol 2014;71(2):158-64. PMID 24366060

Cantu C, Arauz A, Murillo-Bonilla LM, Lopez M, Barinagarrementeria F. Stroke associated with sympathomimetics
contained in over-the-counter cough and cold drugs. Stroke 2003;34(7):1667-72. PMID 12791938

Chamorro A, Vila N, Obach V, Macho J, Blasco J. A case of cerebral hemorrhage early after carotid stenting. Stroke
2000;31:792-3. PMID 10700520

Chen M, Wang Q, Zhu W, et al. Stereotactic aspiration plus subsequent thrombolysis for moderate thalamic
hemorrhage. World Neurosurg 2012;77(1):122-9. PMID 22115547
Chung CS, Caplan LR, Han W, Pessin MS, Lee KH, Kim JM. Thalamic hemorrhage. Brain 1996:119;1873-86. PMID

Cordonnier C, Klijn CJ, Van Beijnum J, Al-Shahi, Salman R. Radiological investigation of spontaneous intracerebral
hemorrhage. Systematic review and trinational survey. Stroke 2010;41:685-90. PMID 20167915

Crum BA, Wijdicks EF. Thalamic hematoma from a ruptured posterior cerebral artery aneurysm. Cerebrovasc Dis
2000;10:475-7. PMID 11070380

Dahlof B, Devereux RB, Kjeldsen SE, et al. Cardiovascular morbidity and mortality in the Losartan Intervention For
Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol. Lancet 2002;359(9311):995-1003.
PMID 11937178

Davis S, Broderick J, Hennerici M, et al. Hematoma growth is a determinant of mortality and poor outcome after
intracerebral hemorrhage. Neurology 2006;66:1175-81. PMID 16636233

De Reuck J. Dorsal thalamic haemorrhage complicating polyarteritis nodosa: a clinico-pathologic case report. Acta
Neurol Belg 2003;103(1):40-2. PMID 12704983

Dejerine J, Roussy G. Le syndrome thalamique. Rev Neurol (Paris) 1906;14:521-32.

Delgado Almandoz JE, Yoo AJ, Stone MJ, et al. The spot sign score in primary intracerebral hemorrhage identifies
patients at highest risk of in-hospital mortality and poor outcome among survivors. Stroke 2010;41:54-60. PMID

Eker A, Yigitoglu PH, Ipekdal HI, Tosun A. Acute onset of intracerebral hemorrhage due to autonomic dysreflexia. J
Korean Neursosurg Soc 2014;55(5):277-9. PMID 25132935

Evans A, Demchuk A, Symons SP, et al. The spot sign is more common in the absence of multiple prior microbleeds.
Stroke 2010;41:2210-7. PMID 20813999

Fiebach JB, Schellinger PD, Gass A, et al. Stroke magnetic resonance imaging is accurate in hyperacute intracerebral
hemorrhage: a multicenter study on the validity of stroke imaging. Stroke 2004;35(2):502-6. PMID 14739410

Fisher CM. The pathologic and clinical aspects of thalamic hemorrhage. Tr Am Neurol Assoc 1959;84:56-9.

Fisher CM. Pathological observations in hypertensive cerebral hemorrhage. J Neuropathol Exp Neurol 1971;30:536-50.
PMID 4105427

Foix C, Hillemand P. Les syndromes de la région thalamique. Presse Méd 1925;1:113-7.

Fornazzari L, Fischer CE, Ringer L, Schweizer TA. “Blue is music to my ears”: multimodal synesthesias after a thalamic
stroke. Neurocase 2012;18(4):318-22. PMID 22111936

Fukuda H, Munoz D, Macdonald RL. Spontaneous thalamic hemorrhage from a lateral posterior choroidal artery
aneurysm: case report. World Neurosurg 2013;80(6):900.e1-6. PMID 23396071

Hallevi H, Abraham AT, Barreto AD, Grotta JC, Savitz SI. The spot sign in intracerebral hemorrhage: the importance of
looking for contrast extravasation. Cerebrovasc Dis 2010;29(3):217-20. PMID 20029193

Han YS, Lee E, Kim JS. Horizontal nystagmus and homonymous hemianopia due to lateral geniculate body hemorrhage.
Eur Neurol 2009;61(6):371-3. PMID 19365130

Hemphill JC 3rd, Greenberg SM, Anderson C, et al. Guidelines for the management of spontaneous intracerebral
hemorrhage. A guideline from the American Heart Association/American Stroke Association. Stroke 2015;46:2032-60.
PMID 26022637

Hill MD, Silver FL, Austin PC, Tu JV. Rate of stroke recurrence in patients with primary intracerebral hemorrhage. Stroke
2000;31:123-7. PMID 10625726
Hirano A, Matsui T. Vascular structures in brain tumors. Hum Pathol 1975;6:611-21. PMID 1100515

Hirose G, Kosoegawa H, Saeki M, et al. The syndrome of posterior thalamic hemorrhage. Neurology 1985;35(7):998-
1002. PMID 4010967

Inagawa T, Ohbayashi N, Takechi A, Shibukawa M, Yahara K. Primary intracerebral hemorrhage in Izumo City, Japan:
incidence rates and outcome in relation to the site of hemorrhage. Neurosurgery 2003;53(6):1283-98. PMID 14633295

Karnath HO, Johannsen L, Broetz D, Kuker W. Posterior thalamic hemorrhages induces “pusher syndrome.” Neurology
2005;64(6):1014-9. PMID 15781819

Kase CS, Furlan AJ, Wechsler LR, et al. Cerebral hemorrhage after intra-arterial thrombolysis for ischemic stroke: The
PROACT II trial. Stroke 2001;57:1603-10. PMID 11706099

Kawahara N, Sato K, Muraki M, Tanaka K, Kaneko M, Uemura K. CT classification of small thalamic hemorrhages and
their clinical implications. Neurology 1986;36:165-72. PMID 3945386

Kim JS. Delayed onset mixed involuntary movements after thalamic stroke. Clinical, radiological and pathophysiological
findings. Brain 2001;124:299-309. PMID 11157557

Koga T, Shin M, Maruyama K, Terahara A, Saito N. Long-term outcomes of stereotactic radiosurgery for arteriovenous
malformations in the thalamus. Neurosurgery 2010;67:398-403. PMID 20644425

Kumar S, Selim M, Marchina S, Caplan LR. Transient neurological symptoms in patients with intracerebral hemorrhage.
JAMA Neurol 2016;73:316-20. PMID PMID 26747699

Kumral E, Kocaer T, Ertubey NO, et al. Thalamic hemorrhage. A prospective study of 100 patients. Stroke 1995;26:964-
70. PMID 7762047

Kwak R, Kadoya S, Suzuki T. Factors affecting the prognosis in thalamic hemorrhage. Stroke 1983;14:493-500. PMID

Laiwattana D, Sangsawang B, Sangsawang N. Primary multiple simultaneous intracerebral hemorrhages between 1950
and 2013: analysis of data on age, sex and outcome. Cerebrovasc Dis Extra 2014;4(2):102-14. PMID 24932180

Leker RR, Khoury ST, Rafaeli G, et al. Prior use of statins improves outcome in patients with intracerebral hemorrhage:
prospective data from the National Acute Stroke Israeli Surveys (NASIS). Stroke 2009;40(7):2581-4. PMID 19407227

Lhermitte J. Les syndromes thalamiques dissociés: les formes analgique et hémialgique. Ann Méd 1925;17:488-501.

Li L, Yin J, Li Y, et al. Anaplastic astrocytoma masquerading as hemorrhagic stroke. J Clin Neurosci 2013;20(11):1612-4.
PMID 23510543

Li N, Wang Y, Wang W, et al. Contrast extravasation on computed tomography angiography predicts clinical outcome
in primary intracerebral hemorrhage: a prospective study of 139 cases. Stroke 2011:32:3441-6. PMID 21980207

Li Q, Zhang G, Xiong X, et al. Black hole sign: novel imaging marker that predicts hematoma growth in patients with
intracerebral hemorrhage. Stroke 2016;47(7):1777-81. PMID 27174523

Macellari F, Paciaroni M, Agnelli G, Caso V. Neuroimaging in intracerebral hemorrhage. Stroke 2014;45(3):903-8. PMID

Maeshima S, Osawa A, Yamane F, Ishihara S, Tanahashi N. Dysphagia following acute thalamic haemorrhage: clinical
correlates and outcomes. Eur Neurol 2014;71(3-4):165-72. PMID 24457317

Masdeu JC, Gorelick PB. Thalamic astasia: inability to stand after unilateral thalamic lesions. Ann Neurol 1988;23:596-
603. PMID 2841901

Matsuyama T, Okuchi K, Nogami K. Protein C deficiency presenting a thalamic hemorrhage. Am J Emerg Med
2002;20:381-2. PMID 12098199
Mayer SA, Brun NC, Begtrup K, et al. Efficacy and safety of recombinant activated factor VII for acute intracerebral
hemorrhage. N Engl J Med 2008;358:2127-37. PMID 18480205

Mayer SA, Davis SM, Skolnick BE, et al. Can a subset of intracerebral hemorrhage patients benefit from hemostatic
therapy with recombinant activated factor VII. Stroke 2009;40(3):833-40. PMID 19150875

Mendelow AD, Gregson BA, Fernandes HM, et al. Early surgery versus initial conservative treatment in patients with
spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral Haemorrhage
(STICH): a randomised trial. Lancet 2005;365:387-97. PMID 15680453

Meretoja A, Churilov L, Campbell BC, et al. The spot sign and tranexamic acid on preventing ICH growth- AUStralasia
Trial (STOP-AUST): protocol of a phase II randomized, placebo-controlled, double blind, multicenter trial. Int J Stroke
2014;9(4):519-24. PMID 23981692

Messe SR, Cucchiara BL. Wrong-way eyes with thalamic hemorrhage. Neurology 2003;60:1524. PMID 12743243

Morita A, Kelly PJ. Resection of intraventricular tumors via a computer-assisted volumetric stereotactic approach.
Neurosurgery 1993;32:920-7. PMID 8327092

Nakajima M, Sugano H, Iimura Y, et al. Sturge-Weber syndrome with spontaneous intracerebral hemorrhage in
childhood. J Neurosurg Pediatr 2014;13(1):90-3. PMID 24160667

Osawa A, Maeshima S, Yamane F, et al. Agraphia caused by left thalamic hemorrhage. Case Rep Neurol 2013;5(1):74-
80. PMID 23620716

Paciarioni M, Bogousslavsky J. Pure sensory syndromes in thalamic stroke. Eur Neurol 1998;39:211-7. PMID 9635471

Pan C, Hu Y, Liu N, et al. Aggressive blood pressure lowing therapy in patients with acute intracerebral hemorrhage is
safe: a systematic review and meta‑analysis. Chin Med J (Engl) 2015;128:2524-9. PMID 26365973

PROGRESS Collaborative Group. Randomised trial of a perindopril-based blood-pressure-lowering regimen among 6105
individuals with previous stroke or transient ischaemic attack. Lancet 2001;358:1033-41. PMID 11589932

Ramanan M, Shankar A. Minimally invasive surgery for primary supratentorial intracerebral haemorrhage. J Clin
Neurosci 2013;20(12):1650-8. PMID 24161339

Remes-Troche JM, Téllez-Zenteno JF, Rojas-Serrano J, Senties-Madrid H, Vega-Boada F, García-Ramos G. Thalamic and
mesencephalic hemorrhages after multiple honeybee stings: a life-threatening apitherapy complication. Eur Neurol
2003;49(3):188-9. PMID 12646770

Saeki N, Nakazaki S, Kubota M, et al. Hemorrhagic type Moyamoya disease. Clin Neurol Neurosurg 1997;99(Suppl
2):S196-201. PMID 9409437

Samadani U, Rohde V. A review of stereotaxy and lysis for intracranial hemorrhage. Neurosurg Rev 2009;32(1):15-22.
PMID 18830646

Sarkar J, Naik B, Gawande A, Goel A. Vivax malaria: a rare cause of thalamic bleed. Asian Pac J Trop Med
2012;5(8):665-6. PMID 22840458

Sasaki T, Kurita H, Saito I, et al. Arteriovenous malformations in the basal ganglia and thalamus: management and
results in 101 cases. J Neurosurg 1998;88(2):285-92. PMID 9452237

Schellinger PD, Fiebach JB, Hoffmann K, et al. Stroke MRI in intracerebral hemorrhage: is there a perihemorrhagic
penumbra. Stroke 2003;34(7):1674-9. PMID 12805502

Shah SD, Kalita J, Misra UK, Mandal SK, Srivastava M. Prognostic predictors of thalamic hemorrhage. J Clin Neurosci
2005;12:559-61. PMID 15936200

Shimohata M, Watanabe Y, Tanaka H. Numbness in the tip of the tongue and lower lip caused by thalamic hemorrhage.
J Stroke Cerebrovasc Dis 2014;23(3):557-9. PMID 23602113
Skidmore FM, Williams LS, Fradkin KD, Alonso RJ, Biller J. Presentation, etiology, and outcome of stroke in pregnancy
and puerperium. J Stroke Cerebrovasc Dis 2001;10(1):1-10. PMID 17903792

Stefani MA, Porter PJ, terBrugge KG, Montanera W, Willinsky RA, Wallace MC. Large and deep brain arteriovenous
malformations are associated with risk of future hemorrhage. Stroke 2002;33:1220-4. PMID 11988594

Steinke W, Sacco RL, Mohr JP, et al. Thalamic stroke. Presentation and prognosis of infarcts and hemorrhages. Arch
Neurol 1992;49:703-10. PMID 1497496

Terao T, Takahashi H, Yokochi F, Taniguchi M, Okiyama R, Hamada I. Hemorrhagic complication of stereotactic surgery
in patients with movement disorders. J Neurosurg 2003;98(6):1241-6. PMID 12816271

Thompson AL, Kosior JC, Gladstone JC, et al; for the PREDICT/Sunnybrook ICH CTA Study Group. Defining the CT
angiography ‘spot sign' in primary intracerebral hemorrhage. Can J Neurol Sci 2009;36:456-61. PMID 19650356

Tokgoz S, Demirkaya S, Bek S, et al. Clinical properties of regional thalamic hemorrhages. J Stroke Cerebrovasc Dis
2013;22(7):1006-12. PMID 22579448

Tsivgoulis G, Katsanos AH, Butcher KS, et al. Intensive blood pressure reduction in acute intracerebral hemorrhage: a
meta-analysis. Neurology 2014;83(17):1523-9. PMID 25239836

Wang WZ, Jiang B, Liu HM, et al. Minimally invasive craniopuncture therapy vs. conservative treatment for
spontaneous intracerebral hemorrhage: results from a randomized clinical trial in China. Int J Stroke 2009;4(1):11-6.
PMID 19236490

Young WB, Lee KP, Pessin MS, Kwan ES, Rand WM, Caplan LR. Prognostic significance of ventricular blood in
supratentorial hemorrhage: a volumetric study. Neurology 1990;40:616-9. PMID 2320234

Zesiewicz TA, Sullivan KL, Hoffmann SM, et al. Delayed thalamic intracranial hemorrhage in an essential tremor patient
following deep brain stimulation. Eur Neurol 2008;59:187-9. PMID 18230878

**References especially recommended by the author or editor for general reading.

Former authors

Janet Wilterdink MD (original author)

ICD and OMIM codes

ICD codes

Intracerebral hemorrhage: 431

Intracerebral hemorrhage: I61.9


Age range of presentation

0-01 month
01-23 months
02-05 years
06-12 years
13-18 years
19-44 years
45-64 years
65+ years
Sex preponderance


Family history




Population groups selectively affected

none selectively affected

Occupation groups selectively affected

none selectively affected

Differential diagnosis list

cerebral infarction
cerebral hemorrhage

Associated disorders

Arteriovenous malformation
Bleeding diathesis
Cerebral infarction
Cerebral neoplasm
Pusher syndrome

Other topics to consider

Basal ganglia hemorrhage

Hypertensive intracerebral hemorrhage
Lobar hemorrhage
Nontraumatic intracerebral hemorrhage
Rostral brainstem and thalamic infarctions
Vertical gaze palsy

Copyright© 2001-2016 MedLink Corporation. All rights reserved.