Thalamic hemorrhages are a common form of intracerebral hemorrhage, and usually are a result of poorly controlled long-standing hypertension, although also have other causes. When due to chronic hypertension, the stigmata of chronic hypertensive encephalopathy are often present (see cerebral microhemorrhages).

The thalamus transmits or prevents transmission of sensory signals from sensory areas of the cerebral cortex through internal capsule fibers and has a role in memory, and thus the clinical presentation reflects this ¹. Thus, the clinical presentation is varied depending on the thalamic nuclei involved ²:

downward gaze (paralysis of upward gaze)
small pupils (lack of light pupillary response)
depressed consciousness
apathy
hypersomnolence
disorientation
visual hallucinations
aphasia
impairment of verbal memory
visuospatial dysfunction
pain and sensory anomalies (including Déjerine-Roussy syndrome)

Thalamic strokes can also present with behavioral patterns depending on the four main arterial thalamic territories:

anterior: preservation, apathy, and amnesia
- paramedian infarction: disinhibition, personality change and amnesia (severe retrograde and anterograde amnesia)
- extensive lesions: "thalamic dementia"
inferolateral: executive dysfunction and occasionally severe long-term disability
posterior: no specific behavioral pattern, however, can include cognitive dysfunction, neglect, aphasia

Radiographic features

Thalamic hemorrhage is easily recognisable on CT as hyperdensity within the thalamus.

There are many predictors of hematoma expansion potentially evident on CT, which are discussed in depth in the main intracerebral hemorrhage article.

Treatment and prognosis

The treatment is no different for other hypertensive strokes. Generally supportive measures are required but control of hypertension and reversal of any anticoagulation is vital.