Thalamic Anatomy and Pathology
|THALAMIC NUCLEI AND THALAMOCORTICAL RADIATIONS|
The thalamus, along with the hypothalamus and subthalamus, form the diencephalon. Anatomically, the thalamus sits above the hypothalamic sulcus in the third ventricle and consists of an egg-shaped structure, one on each side of the brain, connected by a bridge in the middle, the massa intermedia. The thalamus is divided by a white matter sheet known as the internal medullary lamina, into the anterior, medial, and lateral groups of relay nuclei. The lateral group in turn is divided into a ventral tier of nuclei and the lateral nuclei proper. The relay nuclei each projects to a specific territory in the cerebral cortex, and in turn neurons in layer VI of each neocortical area project back to the same specific thalamic relay nucleus. The relay nuclei typically innervate layer IV of the cerebral cortex and provide most of the sensory information to the cerebral cortex.
In addition, there are several cell groups along the midline and embedded in the internal medullary lamina (the intralaminar nuclei). These nuclei send projections more diffusely in the cerebral cortex, with projections favoring layer V, and some project to the striatum as well. They are sometimes viewed as having a more generalized arousal function.
By contrast, the reticular nucleus sits like a thin sheet along the surface of the thalamus. While nearly all of the other thalamic neurons use the excitatory neurotransmitter glutamate, reticular neurons all use GABA and are inhibitory. They sample input both from the cerebral cortex and from the relay nuclei and send inhibitory axons to the relay nuclei, which put the relay neurons into a state where they burst rhythmically but do not transmit sensory information. This bursting behavior underlies the appearance of waxing and waning runs of rhythmic waves in the 12-14 Hz range in the EEG, called “sleep spindles,” as an individual enters slow-wave sleep. It is also thought to be involved in causing the characteristic 3-Hz “spike-and-wave” pattern of EEG seen during “absence” seizures, in which subjects, usually children, lose contact with the external world for brief intervals, during which they may stare and smack their lips. The reticular nucleus is thought to be important in directing attention to discrete sensory stimuli and inhibiting competing stimuli. Among the relay nuclei, the largest component of the anterior group is the anterior nucleus. The most caudal part of the anterior group is called the laterodorsal nucleus. These nuclei send axons mainly to the cingulate gyrus.
The medial group is represented by a single nucleus, the mediodorsal nucleus (MD). MD provides input to the medial and lateral surfaces of the frontal lobe, as well as to much of the temporal lobe.
The lateral group is much more complicated. The ventral tier consists of a series of nuclei related to regions of the motor and sensory cortices. The ventral anterior nucleus (VA) receives input from the globus pallidus internal segment and the substantia nigra pars reticulata, concerned with initiation of movement, and projects to the premotor cortex. The ventro- lateral nucleus (VL) is the terminus of the cerebellar output (the dentatorubrothalamic tract), which carries information about body movement and innervates the primary motor cortex. The ventroposterior lateral nucleus (VPL) receives sensory input from the spinal cord for the arms, legs, and trunk, and the ventroposterior medial nucleus (VPM) serves the same function for the face. They project topographically to the primary somatosensory cortex. Just medial to VPM is the ventroposteromedial parvicellular nucleus, a small area (not pictured here) that receives taste information from the tongue and projects to a gustatory region in the anterior insular cortex. Most caudally in the ventral tier are the medial geniculate nucleus, which conveys auditory information from the inferior colliculus to the primary auditory cortex, and the lateral geniculate nucleus, which relays visual information from the optic tract to the primary visual cortex.
The dorsal tier of the lateral group includes a series of nuclei that project to progressively more posterior parts of the parietal lobe temporal lobe. The lateroposterior nucleus (LP) and posterior nucleus (PO) send axons to the region just caudal to the primary somatosensory cortex. The pulvinar nucleus sends axons to the posterior parietal lobe and the lateral surface of the temporal lobe. The neurons in these cell groups relay integrative information that relates the visual and auditory map of the world to the personal space of the individual.
The most common neurologic disorders involving the thalamus are small infarcts, sometimes called “lacunar infarcts.” These are believed to be due to the occlusion of small thalamic perforating arteries that arise from the posterior cerebral and posterior communicating arteries. The infarctions are often as small as a single nucleus, causing sensory loss on the contralateral body or face if the VPL or VPM nuclei are damaged; memory impairment if the MD and anterior nuclei are involved; or motor weakness if the VL or VA nuclei are injured. The lateral geniculate nucleus may be involved by an occlusion of the anterior choroidal artery, resulting in homonymous hemianopsia. After a pure sensory thalamic infarct involving VPL or VPM, some patients go on to develop pain in the deprived region, known as the Dejerine-Roussy syndrome.
The thalamic perforating arteries may also hemorrhage. This often produces a thalamic syndrome similar to ischemic infarction. However, as the hemorrhage grows it may press downward on the midbrain, causing impairment of consciousness or a cluster of eye movement problems known as Parinaud syndrome. In Parinaud syndrome there is loss of pupillary light reflexes, upgaze, and vergence eye movements due to pressure on the pretectal area and dorsal midbrain.
|AXIAL (HORIZONTAL) SECTIONS THROUGH THE FOREBRAIN:|
LEVEL 6 — CAUDATE AND MID-THALAMUS
The thalamus is also characteristically involved in fatal familial insomnia, a prion disorder that causes rapid onset of dementia, ataxia, and brainstem dysfunction, including almost complete inability to sleep in some cases. However, the pathology involves the cerebral cortex and brainstem as well, and it is difficult to determine how much of the symptomatology is due to the thalamic degeneration. Eastern equine encephalitis also preferentially involves the thalamus and basal ganglia.