1.- Introduction. Anatomy

The basal ganglia and thalamus are bilateral and paired central deep gray matter structures involved in motor, executive, behavioral and cognitive functions. 

The basal ganglia are a group of interconnected nuclei located deep within the cerebral hemispheres and have connections to the cerebral cortex, thalamus and brainstem. They include the caudate nucleus, putamen, globus pallidus, subthalamic nucleus and substantia nigra.

The lenticular nucleus (anatomical and functional unit formed by the globus pallidus and the putamen) has a high metabolic rate, requiring an increased supply of glucose and oxygen, which makes it more vulnerable to metabolic and systemic processes.

The thalamus is a midline structure located between the cerebral hemispheres and the midbrain. It consists of multiple nuclei that relay sensory and motor signals to the cerebral cortex and plays a crucial role in the regulation of consciousness, sleep and alertness.

The basal ganglia and thalami, due to their complex anatomy and strategic location, are key structures in normal neurological function and can be affected by various pathological conditions, many of which are commonly evaluated through radiological imaging. Magnetic resonance imaging (MRI) is the modality of choice, as it provides superior soft tissue contrast and detailed visualization of structural abnormalities. However, computed tomography (CT) is typically the initial imaging technique in acute clinical scenarios due to its rapid acquisition and availability.

2.- Physiological Conditions of the Basal Ganglia and Thalamus

There are several physiological conditions or normal variants of the basal ganglia and thalami that are common and important to recognize to avoid confusing them with pathological abnormalities. The three most relevant are:

• Calcifications: Bilateral and symmetrical calcifications, particularly in the globus pallidus, result from colloid deposition around small cerebral vessels, later undergoing calcification. In individuals over 40, they are often considered physiological. However, basal ganglia calcifications can be associated with various pathologies like hypoparathyroidism, Fahr disease or toxoplasmosis. Therefore, in patients under 40 or with calcifications in other brain regions, underlying pathology should be investigated.
• Dilatation of the perivascular spaces of Virchow-Robin (VRS): These are fluid-filled spaces that surround blood vessels as they extend from the subarachnoid space into the brain parenchyma. Their size and frequency increase with age. On CT, they appear as small (<1 cm), hypodense, rounded or oval structures without mass effect or edema. On MRI, they have the same signal intensity as cerebrospinal fluid across all sequences. Dilated VRS are classified into three types: Type I (basal ganglia, around lenticulostriate arteries), Type II (subcortical white matter) and Type III (midline, infra- and supratentorial).
• Cerebral iron accumulationn: Pathological iron accumulation in the brain causes tissue damage and impacts disease prognosis, making it essential to recognize normal distribution patterns. On long TR and TE sequences, ferric iron appears as T2 hypointensities. Physiological T2 hypointensities occur in the globus pallidus in middle-aged and elderly adults, in the putamen after 60, but should not appear in the thalamus or caudate at any age.

3.- Pathological Conditions of the Basal Ganglia and Thalamus

Basal ganglia and thalamus abnormalities may be asymmetrical (most commonly seen in neoplasm, infections, vascular/ischemic) or symmetrical (most commonly associated with metabolic, degenerative and congenital diseases, as well as toxic poisoning). The thalamus is usually affected focally by non systemic diseases. 

We present and illustrate a series of cases of these abnormalities evaluated by CT and MRI. 

• HYPOXIC ISCHEMIC ENCEPHALOPATHY (HIE)

HIE is a severe brain injury caused by reduced oxygen and blood flow to the brain, often due to cardiac arrest, respiratory failure, stroke, or other conditions causing prolonged oxygen deprivation. It leads to neuronal damage, which can result in long-term neurological deficits or death.

Imaging Findings: In the early stages CT may appear normal, but as injury progresses, signs such as diffuse cerebral edema or loss of gray-white matter differentiation can be seen. Severe cases may show hypodensity in the basal ganglia and thalami. MRI is more sensitive for detecting early changes: DWI is the most useful sequence, showing restricted diffusion in the cortex, basal ganglia, thalami, and hippocampi. Severe cases can progress to cortical laminar necrosis as T1 hyperintensity in the cortical ribbon.  [fig]1

• CARBON MONOXIDE POISONING (CO)

CO toxicity is a form of toxic encephalopathy caused by inhalation of CO gas, which binds to hemoglobin, reducing oxygen delivery to tissues and leading to hypoxia. The brain, particularly regions with high metabolic demand as basal ganglia, is highly susceptible to damage.

Imaging findings: Early CT scans may appear normal or show hypodensity in the globus pallidus and severe cases may reveal diffuse cerebral edema. MRI is more sensitive: DWI shows restricted diffusion in the globus pallidus, subcortical white matter, and hippocampi in acute stages. Chronic cases can develop gliosis and atrophy, particularly in the basal ganglia and white matter.  [fig]2

• OSMOTIC MYELINOLYSIS SYNDROME

Osmotic myelinolysis is caused by rapid shifts in serum osmolality, most commonly due to the rapid correction of severe hyponatremia. It leads to demyelination in specific brain regions, primarily the central pontine myelinolysis in the pons, but can also affect extrapontine areas such as the basal ganglia, thalami and subcortical white matter. 

Imaging findings: Early CT findings may be subtle or absent. In later stages, hypodense lesions in the pons or other affected areas may appear. MRI is the preferred modality: T2/FLAIR sequences show hyperintense lesions in the central pons, often sparing the peripheral fibers, giving a characteristic "trident" or "batwing" appearance. Extrapontine involvement can also be seen in the basal ganglia, thalami, and subcortical white matter. DWI may show restricted diffusion in the acute phase, while chronic cases may develop atrophy and gliosis.  [fig]3

• ACQUIRED HEPATOCEREBRAL DEGENERATION

Hepatocerebral degeneration is a rare neurological disorder that occurs in patients with chronic liver disease. It results from the accumulation of neurotoxic substances, such as ammonia and manganese, leading to progressive neurological deterioration including movement disorders, cognitive impairment and psychiatric symptoms.

Imaging findings: CT scans usually don’t show specific signs, but in advanced cases, mild brain atrophy may be present. MRI is the best tool: the most common finding is bilateral symmetric T1 hyperintensity in the globus pallidus caused by manganese accumulation. Other affected areas can include the substantia nigra, midbrain, and cerebellum.  [fig]4

• DIABETIC STRIATOPATHY

Diabetic striatopathy is a rare neurological complication of poorly controlled diabetes. It primarily affects the basal ganglia, leading to movement disorders such as hemichorea-hemiballismus.

Imaging findings: In CT, the most characteristic finding is unilateral or bilateral hyperdensity in the basal ganglia (particularly in the putamen and caudate nucleus) without mass effect or edema. MRI T1-weighted images show hyperintensity in the affected basal ganglia, while T2/FLAIR may appear normal or show mild hyperintensity. DWI usually does not show restricted diffusion, helping differentiate it from ischemic stroke.  [fig]5

• CREUTZFELDT-JAKOB DISEASE (CJD)

CJD is a rare, fatal prion disease that causes rapidly progressive neurodegeneration. It leads to the accumulation of misfolded prion proteins, resulting in spongiform changes, neuronal loss, and gliosis. Clinically, it presents with rapidly progressive dementia, myoclonus, ataxia, and behavioral changes, with most patients deteriorating within months.

Imaging findings: CT findings are often nonspecific or normal in early stages. In later stages, cortical atrophy may be seen. MRI is the most sensitive tool for diagnosis: DWI bilateral cortical ribboning and involvement of the basal ganglia and thalami are characteristic. T2/FLAIR: Hyperintensities in the same regions may be present. In variant CJD (vCJD), the "pulvinar sign" (hyperintensity in the pulvinar nucleus of the thalamus) is a key finding. Later stages may show brain atrophy.  [fig]6

• STATUS EPILEPTICUS 

Status epilepticus is a neurological emergency defined as a prolonged seizure or repeated seizures without full recovery between episodes, typically lasting more than 5 minutes. 

Imaging findings: CT is often normal in early stages but may show cortical swelling, effacement of sulci, or cytotoxic edema in prolonged seizures. In later stages, cortical atrophy may develop. MRI: Restricted diffusion in affected cortical and subcortical regions, especially in the temporal and frontal lobes. T2/FLAIR: Cortical and subcortical hyperintensities due to neuronal injury and edema. T1-weighted images: Can show laminar necrosis in severe or prolonged SE. Basal ganglia and thalamic involvement may be seen in refractory cases.  [fig]7