Thalamus

Relevant Nuclei

The thalamus is complicated. It contains between 38 and 60 unique nuclei, depending on the source. 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 1.). Scroll to the level of the habenulae in the axial plane and draw a horizontal line through them (Figure 2.).

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 3.).

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 4.). 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.

Figure 1.
Figure 2.
Figure 3.
Figure 4. Axial T2 image demonstrates the red nucleus (red) and approximate location of the lateral geniculate nucleus (green). The medical geniculate nucleus is located just posterior and medial to the lateral geniculate nucleus.

question 1


Where is the lesion?
What deficits are expected, motor or sensory?

show answer


Answer:
VPL nucleus of the thalamus.
Sensory deficits. A lesion here may cause Dejerine-Roussy syndrome or central post-stroke pain (CPSP), characterized by hypersensitivity to pain.

Explanation:
Note the ovoid T2 hyperintensity in the right thalamus. Draw a horizontal line through the habenulae. The bright spot is centered within the lateral most nucleus that is sitting on top of the habenula line; the VPL. This area has reciprocal connections with the somatosensory cortex, so sensory deficits are expected. More about this in the next section.

question 2


What nucleus does this lesion involve?
What deficits are expected?

show answer


Answer:
Left LGN.
Visual deficits.

Explanation:
The left coronal T2 shows a focal hyperintensity superior and medial to the left hippocampus. In the same patient, the right axial FLAIR shows a focal hyperintensity lateral to the red nucleus in the expected position of the LGN. Visual deficits are expected, classically a contralateral homonymous hemianopia.

More on the function of the LGN in the next section.

Function

Sensory

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 5.).

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.

Motor

The VL transmits motor information from the basal ganglia and cerebellum to the motor, pre-motor, and supplemental motor cortices (Figure 6.).

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 7.). As a result, the VA is involved in higher order motor function and motor decision making.

Figure 5.
Figure 6.
Figure 7.

Higher order/associative

The AN transmits information from the hippocampus and mamillary bodies via the mammillothalamic tract to the cingulate gyrus (Figure 8.), which is an important pathway for memory and a component of the Papez circuit (Figure 9.).

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 10.).

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.

Figure 8.
Figure 9.
Figure 10.

question 3


A 35 year-old right-handed male presents with aphasia.

Where is the lesion?
Can you make sense of why he has aphasia?

show answer


Answer:

Left dorsomedian (DM) nucleus.

The DM connects to the prefrontal cortex, including to Broca's area. A left-sided DM lesion in a right-handed person may cause an expressive aphasia, because the relay station between what you want to say and the muscles required to say it is damaged.

The pulvinar connects to the parieto-temporal association cortex, including to Wernicke's area.  A left pulvinar lesion may cause a fluent aphasia, because the relay station between what you hear and how you interpret it is damaged.

***
Note this is a simplified model for conceptualizing language, and modern theories support distributed cortical networks over language processing being confined to focal Broca's and Wernicke's areas.

T2 weighted image with a lesion in the left DM nucleus.
T2 weighted MRI showing the connection of the pulvinar to Wernicke's area and the DM nucleus to Broca's area.

question 4


A 51-year-old woman presents with somnolence, double vision, and impaired memory.

Where is the lesion?

show answer


Answer:


Right DM.

These are some of the classically described symptoms of a right DM lesion.

T2 weighted image with a lesion in the right DM.

functional neurosurgery

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.

Essential tremor and Parkinson disease

Thalamic target(s): Ventral intermediate nucleus (VIM).

See Figures 11 and 12 for an example of an appropriately positioned ablation zone in the left VIM, achieved with MRgFUS.

Seizures

Thalamic target(s): Centromedian (CM) and anterior nuclei (AN).

Figure 11.
Figure 12. Zoomed in version of Figure 11 depicting the approximate location of the ventral intermediate nucleus (VIM; yellow circle), corresponding to the area of the lesion, located on the inferior border of the ventral lateral nucleus (VL; purple), superior to the ventral posterolateral nucleus (VPL; blue). Note the horizontal yellow line through the habenulae, discussed in the first section.

Vascular Anatomy

Arterial

The thalamus is often described as having four vascular territories: the tuberothalamic, inferolateral, paramedian, and posterior territories (Figure 11). 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 or posterior cerebral arteries. 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.

Venous

Venous drainage of the thalamus occurs through small perforating veins arising from the paired internal cerebral veins and basal vein of Rosenthal (Figure 12.).

Figure 13.
Figure 14.

question 5


Returning to the image from Question 1, which demonstrates a lesion in the right VPL. An occlusion of which artery could cause this lesion?

show answer


Answer:
Right thalamogeniculate artery.

Explanation:
The VPL is located in the inferolateral territory, which is typically supplied by the thalamogeniculate artery arising from the PCA (Figure 13.).  Recall an infarct here is classically associated with Dejerine-Roussy syndrome, more recently referred to as central post-stroke pain (CPSP).

question 6


20-day-old girl presenting with a seizure after a few days of fuzziness and vomiting.

What is the etiology of this finding?

show answer


Answer:


Venous infarct with hemorrhagic conversion.

Left: GRE sequence with susceptibility artifact in the left thalamus and occipital horn of the left ventricle, representing hemorrhage.

Right: Saggital T1 with hyperintensity in the superior saggital sinus, straight sinus, vein of galen, and internal cerebral veins, representing thrombosis.

T2 weighted image with a lesion in the right DM.T2 weighted image with a lesion in the right DM.

Variants

The paramedian arteries have variable origins with four types (Figures 13-16.). Type I is considered normal, where each paramedian artery arises from the ipsilateral PCA (Figure 14). Type IIa results in the paramedian territories being supplied by one PCA, but through separate trunks (Figure 15). Type IIb, also known as the artery of Percheron, results in the paramedian territories being supplied by one PCA through a single trunk (Figure 16.). Type III results in both paramedian arteries arising from a bridging vessel between the PCAs (Figure 17).

Artery of Percheron Infarct

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 18). 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. More on this in the next section.

Figure 14.
Figure 15.
Figure 16.
Figure 17.
Figure 18.

Bilateral thalamic lesions


Bithalamic lesions are uncommon, but it is worthwhile knowing a differential for when they arise. Imaging findings can be very nonspecific. To make a diagnosis, you will need to use the clinical history and whether additional areas of the brain are involved. The distribution of the signal abnormality within the thalamus may also help in narrowing a differential (Figure 19).

Figure 19. CJD: Creutzfeldt-Jakob disease, ADEM: acute disseminated encephalomyelitis, PRES: posterior reversible encephalopathy syndrome, DM: dorsomedian nucleus.

cASE 1


32-year-old woman with difficulty walking, hallucinations, agitation, and fevers after returning from the Philippines. What is the top differential? 

show answer


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.

Figure 20.

cASE 2


48-year-old man with uncontrolled hypertension presents with altered mental status and visual disturbances. Top differential?

show answer


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.

Figure 19. Top: FLAIR sequence with symmetric, diffuse, and nonexpansile hyperintensity in the bilateral thalami and periventricular white matter. Bottom: FLAIR sequence with confluent hyperintensity in the occipital lobe.

cASE 3


23-year-old man with history of chronic joint and abdominal pain presenting with progressive tremor, dysarthria, and drooling. Top differential?

show answer


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 21. T2 weighted sequence with nearly symmetric, diffuse, and nonexpansile hyperintensity in the bilateral thalami.

Figure 21.

cASE 4


8-month-old girl with a history of infantile spasms and generalized tonic conic seizures. Top differential?

show answer


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.

cASE 5


24-year-old woman presenting with headache and nausea. What is the top differential? 

show answer


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 22. T2 sequence with symmetric mass-like and expansile hyperintensities in the bilateral thalami.

Figure 22.

cASE 6


47-year-old woman with a history of systemic lupus erythematosis (SLE) and antiphospholipid syndrome (APS) presents with confusion and headache. Top differential?

show answer


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.

cASE 7


38-year-old man with prolonged nausea and vomiting after gastric bypass surgery presents with nystagmus, ataxia, and confusion. Top differential?

show answer


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.

cASE 8


55-year-old man presenting with depression and myoclonus. What sign is this and what diagnosis or diagnoses does it suggest?

show answer


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 23. FLAIR sequence with hyperintensity in the bilateral medial thalami and pulvinar nuclei. There is also hyperintensity of the basal ganglia.

Figure 23.

Summary

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 symptoms, 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.

References and Further Reading