The thalamus is complicated. It contains between 38 and 60 unique nuclei, depending on the source. Some of the major ones are depicted in Figure 1. There are nuclei in the thalamus that send and receive signals via tracts that go to specific, localized cortical areas, while others are more diffuse. The function of a nucleus is determined by the strength and location of these connections.
Thalamic nuclei are not well visualized on routine brain MRs, but they can be localized based on a few landmarks. The thalamus is bordered medially by the third ventricle and laterally by the posterior limb of the internal capsule (Figure 2.). Scroll to the level of the habenulae in the axial plane and draw a horizontal line through them (Figure 3.).
The area of the thalamus posterior to the line is called the pulvinar, which means couch or chair lined with pillows in Latin; think of it of the couch that the rest of the thalamus sits on. There are three nuclei that abut the line anteriorly. From lateral to medial, they are the ventral posterolateral (VPL) nucleus, centromedian (CM) nucleus, and dorsomedian (DM) nucleus. On top of the VPL sits the ventral lateral (VL) nucleus, and on top of that the ventral anterior (VA) nucleus (Figure 4.). The anterior nucleus (AN) is located one slice superior, with the mammillothalamic tract located inferior (see Figure 10. in the next section).
Another clinically relevant nucleus to recognize is the lateral geniculate nucleus (LGN). Scroll down a few slices to the top of the midbrain at the level of the red nucleus and look lateral (Figure 5.). Alternatively, in the coronal plane, find the red nucleus and scroll 1 slice posterior (assuming 5 mm slice thickness); the LGN is located above and medial to the hippocampus. A third slightly more involved way is to follow the optic chiasm posteriorly until it ends, which provides a hint to the LGN's function.
a. Where is the lesion?
b. What deficits are expected, sensory or motor?
a. What nucleus does this lesion involve?
b. What type of deficits are expected?
The VPL takes sensory information from the medial lemniscus (fine touch, vibration, proprioception) and the spinothalamic tract (crude touch, pain, temperature, and pressure) and connects to the primary somatosensory cortex located in the post-central gyrus (Figure 6.).
The LGN takes sensory information from the retina and connects to the primary visual cortex. The LGN has 6 layers. From dorsal to ventral, the first four are the parvocellular layers (parvo = small) which have inputs from retinal midget cells (form and color). The bottom two are magnocellular layers which have inputs from retinal parasol cells (motion).
The medial geniculate nucleus (MGN), located slightly posterior and medial to the LGN, transmits auditory information to the auditory cortices.
The VL transmits motor information from the basal ganglia and cerebellum to the motor, pre-motor, and supplemental motor cortices (Figure 7.).
The VA transmits motor information from the basal ganglia and deep cerebellar nuclei diffusely to the cortex of the frontal lobe, including motor cortices like the VL but also to the prefrontal cortex (Figure 8.). As a result, the VA is involved in higher order motor function and motor decision making.
The AN transmits information from the hippocampus and mamillary bodies via the mammillothalamic tract to the cingulate gyrus (Figure 9.), which is an important pathway for memory and a component of the Papez circuit (Figure 10.).
The DM transmits information between the amygdala, limbic basal ganglia, and olfactory cortex to the prefrontal association cortex. It is important in memory, attention, and higher order functions (Figure 11.).
The pulvinar transmits information between the tectum and the parietotemporal-occipital association cortex. It is important in the processing of visual information and attention.
The CM transmits information diffusely between the basal ganglia, cortex, and brainstem. It is important in arousal, motor coordination, and pain processing.
A 83 year-old-woman presents with status epilepticus.
a. What thalamic nucleus is involved?
A 35 year-old right-handed male presents with aphasia.
a. Where is the lesion?
b. How does the location of this lesion relate to aphasia?
A 51-year-old woman presents with somnolence, double vision, and impaired memory.
a. Where is the lesion?
The thalamus is an excellent target for stimulation (deep brain stimulation (DBS)) and ablation (stereotactic radiosurgery (SRS), radiofrequency (RF), MR guided focused ultrasound (MRgFUS), or laser interstitial thermal therapy (LITT)) for the treatment of neurological and psychiatric disorders gives its wide array of functions and connectivity throughout the brain.
Thalamic target(s): Ventral intermediate nucleus (VIM).
See Figure 12. and Figure 13. for an example of an appropriately positioned ablation zone in the left VIM, achieved with MRgFUS.
Thalamic target(s): Centromedian (CM) and anterior nuclei (AN).
See Figure 14. for an example of CM nucleus DBS lead placement for the treatment of drug-resistant epilepsy. Reflecting its function, CM stimulation also increases arousal, a welcome effect given the prevalence of epileptic encephalopathy in these patients.
The thalamus is often described as having four vascular territories: the tuberothalamic, inferolateral, paramedian, and posterior territories (Figure 15.). Arterial supply to thalamus is highly variable. Often the arteries supplying the thalamus are clustered in groups of small perforators, each originating from the posterior communicating (PCOM) arteries or posterior cerebral arteries (PCA). In other people, these smaller vessels may arise from a single arterial trunk; in this case, a proximal occlusion may lead to infarction of an entire vascular territory.
The lateral thalamus also receives partial blood supply from the anterior choroidal artery, which usually arises from the posterior wall of the distal internal carotid artery; recall an anterior choroidal artery occlusion can infarct the LGN (Question 2). However, the majority of thalamic blood supply comes from the posterior circulation.
Venous drainage of the thalamus occurs through small perforating veins that converge on the paired internal cerebral veins and basal vein of Rosenthal (Figure 16.).
Returning to the image from Question 1, which demonstrates a lesion in the right ventral posterolateral (VPL) nucleus.
a. An occlusion of what artery could cause this lesion?
20-day-old girl presenting with a seizure after a few days of fuzziness and vomiting.
a. What is the diagnosis?
The paramedian arteries have variable origins with four types (Figures 16-19.). Type I is considered normal, where each paramedian artery arises from the ipsilateral PCA (Figure 17.). Type IIa results in the paramedian territories being supplied by one PCA, but through separate trunks (Figure 18.). Type IIb, also known as the artery of Percheron, results in the paramedian territories being supplied by one PCA through a single trunk (Figure 19.). Type III results in both paramedian arteries arising from a bridging vessel between the PCAs (Figure 20.). There is also variability in the extent of each vascular territory. Like the balance between the medial and lateral lenticulostriate vessels in the anterior circulation, or the arteries that supply the cerebellum in the posterior circulation, there is a balance between the arteries that supply the thalamus. For example, the tuberothalamic (anterior) territory may receive the majority or all of its blood supply from the paramedian arteries, especially if the tuberothalamic artery is small or absent. Since the paramedian arteries arise from the PCOM, a hypoplastic or absent PCOM, which is a frequent finding on vascular imaging, likely contributes to this territorial variance.
With the Percheron variant, an occlusion of the single trunk or the PCA proximal to its origin may result in an infarction of the bilateral DM nuclei, or paramedian territories, as shown on the T2 weighted image to the right (Figure 21.). Importantly, the infarct will be centered around and relatively confined to the DM nuclei. If there is diffuse involvement of the thalami bilaterally, the differential is broad but should not include an artery of Percheron infarct. The infarct may extend to the anterior nuclei (see the previous paragraph), but the entire thalamus should not be involved. There may be involvement of the superior midbrain (Figure 22.), termed the "V-sign," which can help narrow the differential when present. More on the differential for bilateral thalamic lesions in the next section.
a. What anatomic variant is present?
32-year-old woman with difficulty walking, hallucinations, agitation, and fevers after returning from the Philippines. What is the top differential?
Answer: Viral or autoimmune encephalitis
Final diagnosis: Japanese encephalitis
Many viral encephalitides may have the same appearance; for example, other Flaviviruses (West Nile, Dengue, etc.) and Ebstein Barr. Autoimmune encephalitis remains a differential consideration, especially in a young female patient.
Figure 20. FLAIR sequence with symmetric, diffuse, and nonexpansile hyperintensity in the bilateral thalami.
48-year-old man with uncontrolled hypertension presents with altered mental status and visual disturbances. Top differential?
Answer: Posterior reversible encephalopathy syndrome (PRES)
PRES is characterized by reversible vasogenic edema, most commonly triggered by hypertension exceeding autoregulation capabilities or endothelial dysfunction from chemotherapy, immunosuppressants, or other toxins. Note the characteristic involvement of the occipital lobes, which may be due to relatively little sympathetic innervation of the posterior circulation.
Image 1: FLAIR sequence with symmetric, diffuse, and nonexpansile hyperintensity in the bilateral thalami and periventricular white matter.
Image 2: FLAIR sequence with confluent hyperintensity in the occipital lobe.
23-year-old man with history of chronic joint and abdominal pain presenting with progressive tremor, dysarthria, and drooling. Top differential?
Answer: Metabolic
Final diagnosis: Wilson disease
Wilson disease results from impaired copper metabolism and deposition in the brain, liver, and cornea. In the brain, imaging findings progress in a somewhat predictable pattern, first and most commonly affecting the putamen. Thalamus and pons involvement tend to be long term sequela.
Figure 23. T2 weighted sequence with nearly symmetric, diffuse, and nonexpansile hyperintensity in the bilateral thalami.
8-month-old girl with a history of infantile spasms and generalized tonic conic seizures. Top differential?
Answer: Vigabatrin toxicity.
Vigabatrin is used to treat infantile spasms and causes a characteristic pattern in the brain with toxicity. Typically, the bilateral thalami, globus pallidus, and brainstem are involved. Findings are reversible with dose lowering or drug cessation.
Image 1: DWI sequence with symmetric hyperintensity in the bilateral thalami.
Image 2: ADC sequence with corresponding hypointensity, consistent with diffusion restriction.
24-year-old woman presenting with headache and nausea. What is the top differential?
Answer: Neoplasm
Final diagnosis: Bithalamic low grade glioma.
Bilateral thalamic gliomas are rare. They are typically low-grade astrocytomas, as was this case, which was non-enhancing on T1 post-contrast images (not included here). They may be symmetric or asymmetric and may spread between the thalami via the interthalamic adhesion, or massa intermedia; a thin band of variably present glial cells linking the thalami.
Figure 24. T2 sequence with symmetric mass-like and expansile hyperintensities in the bilateral thalami.
47-year-old woman with a history of systemic lupus erythematosis (SLE) and antiphospholipid syndrome (APS) presents with confusion and headache. Top differential?
Answer: Deep venous sinus thrombosis.
Occlusion of the internal cerebral veins and vein of Galen classically causes bilateral thalamic infarctions. Anything that results in a prothrombotic state, such as SLE and APS, can predispose to cerebral venous thrombosis. Commonly encountered risk factors include oral contraceptives and the pregnancy/post-partum period.
Image 1: FLAIR sequence with hyperintensity diffusely involving the bilateral thalami.
Image 2: Saggital T1 sequence with hyperintensity in the vein of Galen and internal cerebral veins, consistent with subacute thrombus.
38-year-old man with prolonged nausea and vomiting after gastric bypass surgery presents with nystagmus, ataxia, and confusion. Top differential?
Answer: Wernicke encephalopathy.
Wernicke encephalopathy is caused by thiamine deificiency, most commonly in the setting of alcoholism. However, many cases are non-alcoholic and due to other conditions that predispose to thiamine deficiency, such as hyperemesis gravidarum, cancer, bariatric surgery, etc. It is a clinical diagnosis, but there may be involvement of the medial thalami, periaqueductal gray matter, and rarely but characteristically the mamillary bodies.
Image 1: FLAIR sequence with hyperintensity involving the medial thalami.
Image 2: FLAIR sequence with hyperintensity involving the periaqueductal gray matter.
55-year-old man presenting with depression and myoclonus. What sign is this and what diagnosis or diagnoses does it suggest?
Answer: Hockey stick sign, suggesting Creutzfeldt-Jakob disease (CJD) or possibly Wernicke encephalopathy
Final diagnosis: Sporadic CJD
The majority of CJD cases are sporadic, however the familial variant accounts for approximately 5-15% of cases. Extremely rarely, cases may be iatrogenic, related to exposure to prions either by contact with contaminated materials or in transplants from donors who unknowingly had CJD. The hockey stick sign is most commonly associated with CJD, but Wernicke encephalopathy may cause a similar appearance. The pulvinar sign may be present, referring to hyperintensity of the pulvinar nuclei without involvement of the medial thalami. Basal ganglia and cortical involvement are also prominent features of CJD.
Figure 25. FLAIR sequence with hyperintensity in the bilateral medial thalami and pulvinar nuclei. There is also hyperintensity of the basal ganglia.
The thalamus is complex in both structure and function, playing a role in nearly every way one interacts with the world. Individual thalamic nuclei are not well visualized with current clinical imaging techniques, but their locations can be inferred by surrounding landmarks. Nuclei are involved in sensation (e.g., VPL, LGN, etc.), motor function (e.g., VL, VA. etc.), and higher-order associative functions (e.g., DM, pulvinar, etc.). Damage to these areas may produce predictable results, either as the result of pathology or via ablation for disorders like essential tremor and epilepsy. A wide range of diseases may involve the bilateral thalami, often with significant overlap of imaging features. Nonetheless, this remains a classic differential that is worthwhile to be familiar with. In practice, making a single diagnosis based solely on imaging features is difficult and clinical history is critical for narrowing the differential.