Thalamus · Grey Matter

The thalamus is a pair of egg-shaped masses of grey matter at the centre of the brain through which almost everything that reaches the cortex passes: it relays the senses, the motor loops of the cerebellum and basal ganglia, and the signals that set the level of wakefulness.

Thalamus. The thalamus is a pair of egg-shaped masses of grey matter at the centre of the brain through which almost everything that reaches the cortex passes: it relays the senses, the motor loops of the cerebellum and basal ganglia, and the signals that set the level of wakefulness.

Each thalamus is about 4 cm long and sits on either side of the third ventricle, above the midbrain. It is divided into nuclei, each tied to its own region of cortex in both directions. Vision passes through the lateral geniculate nucleus on its way to the visual cortex, hearing through the medial geniculate nucleus to the primary auditory cortex, touch through the ventral posterior nuclei to the primary somatosensory cortex. Every sense except smell has such a station. Other nuclei carry the loops of the cerebellum and the basal ganglia to the motor cortex, and the anterior nuclei belong to the memory circuit of the limbic system.

It filters as well as relays. The cortex sends more fibres back to the thalamus than it receives from it, and the thin thalamic reticular nucleus around it inhibits the relay cells, so the thalamus can amplify what is attended to and mute the rest.

It sets the brain's state. In deep sleep its cells switch to a bursting mode that produces the slow waves and spindles of the EEG, and widespread rhythmic loops between thalamus and cortex underlie generalised seizures, as the epilepsy card explains.

It also sends a fast, coarse copy of sensory signals directly to the amygdala, the shortcut that lets fear start before the cortex has identified the cause.

Questions: How can you jump at a shape in the grass before you know it is a stick? Sensory signals reach the amygdala by two routes from the thalamus: a short one that goes straight there, and a longer one through the cortex, which identifies the object properly. In rats LeDoux showed that the direct route alone, from the auditory thalamus, is enough to learn and express fear of a sound, and it is faster because it skips the cortical stages. The short route carries a coarse picture (something long, something moving), enough to start a startle and a racing heart; a moment later the cortical route reports that it is a stick, and the prefrontal cortex calms the alarm. Tractography has since traced a matching pathway in humans. Why can a small lesion in the brainstem cause a coma when a large one in the cortex does not? Wakefulness depends on a system of nuclei in the upper brainstem (the reticular activating system with the neuromodulator nuclei near it) that project through the thalamus and the basal forebrain to the whole cortex. All those fibres funnel through a few cubic centimetres of the upper pons and midbrain, so a small stroke or bleed there removes the drive for the entire cortex at once. A cortical lesion, however large, leaves the rest of the cortex awake; in a series of brainstem strokes studied by Parvizi and Damasio, coma followed lesions of the upper pontine and midbrain tegmentum. How does the thalamus help produce the slow waves and spindles of sleep? As arousal falls, the brainstem's neuromodulators withdraw and thalamic relay cells hyperpolarise, which switches them from faithful relaying to rhythmic bursts. The thalamic reticular nucleus, inhibiting the relay cells in rhythm, generates the sleep spindles (bursts of about 11 to 15 Hz), and the loops between thalamus and cortex, together with the cortex's own slow oscillation, produce the large slow waves of deep sleep. In this mode the thalamus transmits little from the senses, which is part of why the sleeping brain is cut off from the world. Why does nearly every sense pass through the thalamus before reaching the cortex? Each sense except smell has a thalamic nucleus that receives it and sends it on to its own area of cortex: the lateral geniculate for vision, the medial geniculate for hearing, the ventral posterior nuclei for touch and taste. Passing everything through one structure lets the brain control the flow, since the cortex sends back more fibres than it receives and the reticular nucleus can mute the relay cells, amplifying what is attended to and damping the rest. The same gate closes in deep sleep, when thalamic cells switch to bursting and the outside world is largely kept out. Where do the signals of the two eyes first meet in a single neuron? Although the chiasm sends both eyes' views of one half-field into the same optic tract, the lateral geniculate nucleus of the thalamus keeps them apart, in separate layers for each eye. The first neurons that respond to both eyes are in the primary visual cortex, beyond its input layer, where the inputs from the two eyes arrive in alternating bands (ocular dominance columns) and then converge. Neurons there are tuned to small differences between the two retinal images, the raw material of stereoscopic depth in the central binocular field, about 120 degrees wide. Why do absence seizures appear as 3 Hz spike-and-wave over both hemispheres at once? The rhythm is generated by a loop between the cortex and the thalamus, which projects to both hemispheres, so the discharge starts everywhere the loop reaches instead of spreading from one spot. Cortex excites the thalamus, the inhibitory neurons of the thalamic reticular nucleus then hyperpolarise the relay cells, and the relay cells answer with a rebound burst carried by T-type calcium channels that drives the cortex again. Each turn of that loop takes about a third of a second, which sets the frequency near 3 per second: the spike is the cortex firing together, the wave is the inhibition that follows. Why does deep brain stimulation for epilepsy target the thalamus? The thalamus is a hub through which seizures spread: its anterior nucleus sits in the circuit linking the hippocampus to the cingulate cortex, so stimulating one small target can influence the wide network that focal seizures, especially temporal ones, travel through. In the randomised trial that led to approval, stimulation of the anterior nucleus reduced seizures 29 % more than sham during the blinded months, and after two years the median reduction was 56 %. The mechanism is still debated, with disruption of the rhythms that recruit the network and gradual changes in the circuit as the main candidates.