The thalamus is a tightly packed collection of nuclei and fibres in the center of the brain that is involved in everything sensory (except olfactory) and extrapyramidally expressive. It is connected to everyone and his mother. Any proper neuropsychological problem can be caused by thalamic lesions – neglect, aphasia, dementia, delirium, visual, sensory, motor disturbances, ataxia, pain. Thus as the caudate nucleus, the thalamus is always a good answer if you are asked for localization of your lesion. It helps immensely to organize the connections and deficits into a simple system in order to understand thalamic stroke deficits. I follow the literature on thalamic strokes and distinguish 4 vascular regions.
The four arteries
Polar artery region (anterior thalamoperforating artery). The anterior nucleus is involved in cognition, episodic memory, language and emotion with connections to the limbic system (the corpora mamillaria, the hippocampus, the cingulum and all else) and the frontal lobes (see this cool article). Together with parts of the lateral nuclei the region is supplied by the A. thalamoperforans anterior (also called polar or tuberothalamic artery) which arises from the mid of the posterior communicating artery, although in about a third of people the paramedian artery replaces it. Strokes in this region are etiologically diverse (as e.g. in the anterior choroidal artery) and lead to thalamic aphasia as well as diverse neuropsychological deficits that resemble caudate strokes, such as change in personality, abulia, apathy and – via its mamillary connections – memory deficits.
Posterior choroidal artery region. This artery arises from (P1 or) P2 and supplies the pulvinar and the geniculate bodies, all of which connect to the auditory (temporal lobe) and visual system (occipital lobe). Resulting deficits are visual field defects (hemianopia, wedge shaped), hearing deficits and more rarely aphasia and other neuropsychological deficits. Since the artery also sometimes reaches the posterior and even lateral ventral nuclei, its occlusion can also lead to hemihypesthesia.
Paramedian artery/arteries. Does the name Percheron ring a bell? He is the one discussing the various anomalies in the paramedian (or posterior thalamoperforating artery): it usually arises from P1 but often one side misses and this side is supplied from the contralateral one, so that a thrombus in one P1 can lead to inferomedial strokes in both thalami (artery of Percheron). As one of the first arteries after the basilar head, basilar artery embolism often leads to paramedian artery and thus to inferomedial thalamic strokes. The most prominent version is Caplan’s top-of-the-basilar-syndrome (a short aside: have you ever read up on the embryology of the vertebrobasilar system? if not – look here).
The artery reaches the medial nuclei (which somehow interact with all other thalamic nuclei) as well as intralaminary nuclei (these lie inside the internal medullary lamina that crosses the thalamus longitudinally), also parts of the pulvinar and sometimes the ventral lateral nuclei. More importantly, a branch of the paramedian artery goes off to the mesencephalon and pons and leads to disturbances in vertical ocular motor control (damaging the rostral = interstitial nucleus of the MLF aka riMLF). In principle a stroke in the paramedian artery can affect the functions of all other thalamic nuclei, but mainly it causes coma or somnolence, vertical gaze paralysis or skew deviation, and neuropschological deficits (“thalamic dementia”).
The thalamogeniculate artery arises from P2 and irrigates the ventral nuclei, including the anterior, lateral, intermediate, posterolateral, posteromedial nuclei. Functionally this implies sensory deficits (hemihypesthesia or hemianalgesia, but also wedge shaped sensory disturbance) via the vental posterolateral (body below face) and ventral posteromedial (trigeminal) nuclei. Interestingly the sensory disturbance in thalamic strokes can be limited exactly in the median (as a counter example for functional deficits) and tends to give rise to intractable pain syndromes (thalamic pain syndrome) later. Through deafferentation the hand moves in a weird dystonic way (with flexion of the wrist and the MCPs, adduction of the thumb and athetosis of the fingers) when the patient is asked to hold up his hands with eyes closed (thalamic hand). Through the ventral anterior and lateral nuclei as well as the subthalamic nucleus connections to the basal ganglia, the premotor cortex and the cerebellum can be harmed – this leads to atactic hemiparesis and hyper- or hypokinetic movement disorders. As the name of the artery suggests, it can also reach the genu and the posterior limb of the capsulae internae, causing the lacunar syndrome sensorimotor hemiparesis. Strokes in this region are – as those in the capsule – mainly (70%) microangiopathic.
The following scheme has been adapted from Powell’s wonderfully concise article:
Specific thalamic syndromes
Thalamic dementia. Although it occurs frequently after paramedian artery strokes, it can also happen in anterior (through the connection to the Hippocampus and Corpora mamillaria) or even medial thalamic lesions. The neuropsychological profile is different from Alzheimer’s and akin to caudate dementia with reduced initiative, recall, short term memory (resembling Korsakoff’s), spontaneity, vigilance. Patients seem indifferent more than incapable of answering. Social intelligence may be affected more severely than formal intelligence.
Thalamic aphasia may be quite diffferent from cortical aphasia; similar to the dementia syndrome patients seem to be less interested in producing speech rather than severely handicapped. Word finding difficulties (as in any aphasia), reduced spontaneous speech, perseverations dominate, with grossly intact grammar and often preserved reading and writing capabilities as well as repetition.
Thalamic sensory deficits. From the full blown syndrome of Déjerine-Roussy with complete hemianesthesia giving way to hypersensitivity, paresthesias and a thalamic pain syndrome to more restricted variants of hypesthesia – dissociated, face or body only, pain only, the lateral thalamic strokes can lead to severely disabling pain syndromes. Sensory deficits can be associated with (usually temporary) hemiparesis (sensorimotor stroke) or atactic hemiparesis.
Thalamic hand. This is more or less a deafferentation syndrome. Without proper feedback on the position of the fingers and hand (eyes closed), the wrist and fingers assume a dystonic posture with flexed wrist, flexed MCPs, straight PIPs and DIPS and hyperadducted thumb. When holding out the hand, deafferentation athetosis may occur, the finger wandering up and down.
- Amici S. Thalamic infarcts and hemorrhages. Front Neurol Neurosci.
2012;30:132-6: a short and concise review – that prefers a triad of arteries.
- Powell R, Hughes T. A chamber of secrets. The neurology of the thalamus:
lessons from acute stroke. Pract Neurol. 2014 Dec;14(6):440-5: as usual, the PN article is witty and to the point – the best english article on thalamic strokes.
- Nolte CH, Endres M, Jungehülsing GJ. Vascular syndromes of the thalamus.
Nervenarzt. 2011 Feb;82(2):231-41: this is in German, but surely the best source ever.