D. Spinal Nucleus and Tract of V
The nucleus and adjacent descending spinal tract of V is to
the face what the spinothalamic tract is to the body. Cell bodies are in the
trigeminal (Gasserian) ganglion, which sits in middle fossa adjacent to brainstem.
Fibers enter at a mid-pons level, descend as far down as the upper cervical cord segments
and synapse in the adjacent spinal nucleus of V. It used to be thought that the
ophthalmic division descended farthest caudally and the mandibular descended least before
synapsing, but this is now disputed. After synapsing, a second-order neuron sends an
axon across the midline to travel close to the medial lemniscus in an indistinct
trigeminothalamic tract (not pictured), ultimately to end in ventral posteromedial
thalamus. A lesion of spinal V in the medulla will cause partial numbness, loss of
pain, and temperature sensation over the ipsilateral half of the face. The blink
reflex is partially mediated by spinal V and partially by main sensory (see below).
E. Nucleus Ambiguus
This nucleus is invisible in adult brain sections but is
clinically well defined and important. In is the analogue of the anterior horn for
the muscles of the pharynx, larynx, derived from branchiomeric arches of old. It
contributes motor fibers to cranial nerves IX (for the stylopharyngeous muscle -- the only
important motor component of IX), X (the main motor nerve to pharynx and larynx), and XI
(for the cranial portion of XI -- fibers destined for the recurrent laryngeal nerve which
will soon join up with the vagus. Recall that the SCM and trapezius are innervated
by the spinal portion of XI or originating in C1-4 special lateral roots joining to ascend
through the foramen magnum, then back out the jugular foramen). A unilateral lesion
of the nucleus ambiguus causes dysphagia, hoarseness, sagging of the ipsilateral palate,
and paresis of the ipsilateral vocal cord. A bilateral lesion may cause failure of
automatic respiration.
F. Nucleus and Tractus Solitarius
The nucleus solitarius is the receiving center for visceral
information, carried predominantly by the vagus nerve. Rostrally, the nucleus
solitarius is called the "gustatory nucleus" as it receives taste inputs from
cranial nerves VII (anterior two-thirds of tongue via chorda tympani), IX (posterior
one-third of tongue), and X (taste buds near epiglottis). It also seems important in
the generation of automatic respiration and control of blood pressure. Isolated
clinical lesions occur very rarely.
G. Hypoglossal (XII) Nucleus
This is the "ventral horn" for the tongue.
Lesions of the nucleus or of the exiting nerve fascicles on the left will cause the tongue
to deviate to the left.
H. Dorsal Motor Vagus (X)
This is one of the main parasympathetic output nuclei of
the body, with the vagus carrying ipsilateral parasympathetic input to glands, heart,
bronchioles, stomach, and proximal bowel. The other parasympathetic centers are in
sacral cord (junction of dorsal and ventral horn around S1-S3), the Edinger-Westphal
nucleus to the pupil via cranial nerve III, and salivatory gland inputs via central nerves
VII and IX.
I. Vestibular Nuclei
The vestibular complex of four nuclei mediates the senses
of static and rotational acceleration. Because the system is close to the cerebellar
peduncles, it is sometimes clinically difficult to distinguish vestibular from cerebellar
deficits. In general, a patient with a left vestibular system lesion will tend to
veer to the left and past-point to the left. A slow drift of the eyes to the left
will be observed with corrective fast-phase nystagmus to the right (nystagmus usually is
named for the direction of the compensatory fast-phase, but this is not always the
case. It is better to specify direction, e.g., "right beating nystagmus."
Involvement of otolith connections might cause strange perceptions of the world tilting:
in response to damaged otolith connections, a skew of the eyes might develop, with the eye
ipsilateral to the lesion usually lower.
J. Reticular Formation
Volumes have been written about the reticular formation,
but requirements for clinical understanding are few. The region of brainstem
influences respiratory rhythms, heart rate, blood pressure, and descending sympathetic
fibers. Collaterals are received from most of the sensory afferent systems.
Influences on the motor system are attempted by reticulospinal control over the gamma-bias
on muscle spindles. Lesions of the descending reticulospinal tracts in the vicinity
of brainstem reticular formation will cause an ipsilateral Horner's syndrome. If a
lesion is bilateral (e.g., cerebellar tonsillar herniation crushing brainstem), vital
functions may suffer.
III. PONS
A. Pontine Nuclei
Cells in the pontine nuclei are the major relay stations
between cerebral cortex and cerebellum. Corticopontine fibers descend in the medial
and lateral thirds of the cerebral peduncles to synapse in the pontine nuclei.
Recipient neurons send axons across the midline to the contralateral middle cerebellar
peduncle and thereby to cerebellar cortex of the lateral hemispheres. The clinical
effects of lesions to this system are uncertain, but new information suggests that
ipsilateral or contralateral cerebellar signs may be produced, depending upon whether the
lesion affects neurons predominantly before or after their decussation.
B. Pontine Corticospinal Tract
These descending fibers have just emerged from the cerebral
peduncles above and are to be gathered into the medullary pyramids below. Their
dispersion is consequent to the prominent pontine nuclei. Lesions at this level
cause contralateral upper motor neuron signs.
C. Medial Lemniscus
This is a continuation of the ascending dorsal column
system. The leg fibers have begun to swing laterally. All sensory afferent
systems traversing the brainstem are in process of migrating laterally and dorsally as
they move toward thalamus.
D. Facial (VII) Nucleus
The facial nucleus is comprised of motor neurons to the
muscles of facial expression. This excludes muscles of mastication, swallowing, and
extraocular movements. Because of the embryonic migration of the nucleus, fibers of
VII have become looped over the VIth nucleus and doubled back on themselves. Lesions
of the facial nucleus or nerve cause ipsilateral paralysis of the muscles of facial
expression. The upper motor neuron innervation to the lower-face portion of the
nucleus is important and contralateral but to the forehead portion, rudimentary.
Because of this quirk, upper motor neuron lesions weaken the lower face more than the
upper face. After the motor fibers of VII exit the brainstem, they are joined by
autonomics to the nasopharynx and salivary glands, by the nerve to stapedius (to dampen
the tympanic membrane in response to loud noises), and by the chorda tympani carrying
taste from the anterior two-thirds of the tongue. Analysis of these associated
functions is helpful in distinguishing pontine disease from a Bell's palsy.
E. Cochlear Nuclei
The dorsal and ventral cochlear nuclei (not shown because
they are slightly caudal to the plane of section) hang suspended over the dorsolateral
pons where it joins the medulla. Afferents are received from the spiral ganglia in
the cochlea. Auditory information passes bilaterally to trapezoid body and superior
olive (it bears no relation functionally to the inferior olive), then via the lateral
lemniscus (not shown) to the medial geniculate body of thalamus. Relays are then
made to the primary auditory cortex deep in the folds of the sylvian fissure
posteriorly. Lesions of the cochlea or VIIIth nerve will cause ipsilateral
deafness. Lesions more centrally will have little clinical effect because of the
bilateral representation of auditory information. Computer-averaged brainstem auditory-
evoked responses to repeated clicks can chart the auditory signal through its course,
thereby serving as a test of "nerve conduction" within the brainstem.
The vestibular component of the VIIIth nerve enters the
pontine and medullary vestibular nuclei discussed above.
F. Main Sensory and Motor Nucleus of V (Trigeminal)
The descending or spinal tract of V, carrying pain and
temperature sensation from the face, was detailed above. Neurons in main sensory V
situated slightly rostral to the plane of section, like those in the spinal nucleus of V,
receive afferents from cells whose bodies lie in the trigeminal ganglion. The main
sensory nucleus of V is equivalent to the dorsal column nuclei as it mediates
discriminative sensation from the ipsilateral face. Efferents cross in the substance
of the pons and ascend in another ill-defined tract to ventroposteromedial thalamus.
Motor V lies just medial to sensory V; it contains lower
motor neurons for the muscles of mastication: masseter pterygoids and temporalis.
The masseters close the jaw, and pterygoids open and protrude the jaw. Since the
pterygoids deviate the jaw to the opposite side as they lower the mandible, a left Vth
palsy will result in jaw deviation to the left upon mouth opening.
Fibers analogous to the spinocerebellar system and
important in mediation of the jaw-jerk reflex originate in the mesencephalic nucleus of V,
located in the lateral boundaries of the fourth ventricle.
The trigeminal complex thus comprises four separate, but
related, nuclei: spinal V for pain and temperature; main sensory V for discriminative
touch; and motor V for jaw power and mesencephalic V for unconscious joint and muscle jaw
sensation.
G. Abducens (VI) Nucleus
Within the abducens nucleus lie two populations of
neurons. Abducens motor neurons project in the VIth cranial nerve to innervate the
ipsilateral-lateral rectus muscle. Abducens internuclear neurons cross the midline
and ascend in the contralateral medial longitudinal fasciculus to the medial rectus
division of the oculomotor nucleus. Thus, the abducens nucleus is responsible for
the yoking of eye movements during conjugate gaze. Lesions of the VIth nerve nucleus
cause a total ipsilateral conjugate gaze palsy. A VIIth nerve palsy is a constant
accompaniment, because the genu of the facial nerve sweeps around the abducens
nucleus. The abducens nucleus receives inputs from the vestibular nuclei and the
adjacent paramedian pontine reticular formation. The paramedian pontine reticular
formation contains cells responsible for saccadic and, probably, pursuit eye
movements. Lesions of the paramedian pontine reticular formation cause a gaze palsy
that may spare vestibular eye movements.
H. Medial Longitudinal Fasciculus
Lesions of the medial longitudinal fasciculus cause
internuclear ophthalmoplegia in which the ipsilateral eye adducts incompletely or slowly
for conjugate eye movements. Vergence eye movements may be normal. Nystagmus
of the other abducting eye is often present; the cause for this is uncertain.
Bilateral internuclear ophthalmoplegia also interferes with vertical vestibular and
pursuit movements, which depend on the medial longitudinal fasciculus; the usual cause is
multiple sclerosis. Unilateral internuclear ophthalmoplegia is usually due to
brainstem infarction.
IV. MIDBRAIN
A. Basis Pedunculi
The basis pedunculi or cerebral peduncles contain
descending corticospinal tract fibers from the ipsilateral hemisphere and descending
corticopontine and corticomedullary fibers. Corticospinal fibers occupy about the
middle one-third, with leg fibers represented most laterally. Corticobulbar (the
bulb is the pons plus the medulla) are just medial to the corticospinal fibers.
Frontopontine fibers occupy the medial one-third and temporoparieto- occipitopontine
fibers, the lateral one-third. In these latter fibers are the connections with the
pontocerebellar nuclei with centers for gaze, with reticuar formation, and other uncertain
systems.
B. Substantia Nigra
The substantia nigra is a gray matter component of the
extrapyramidal motor system. Nigrostriatal fibers containing dopamine are deficient
in Parkinson's disease.
C. Red Nucleus
The red nucleus is another gray matter component of the
extrapyramidal motor system. It gives rise to the rubrospinal tract which crosses
near its origin in midbrain and descends just ventral to the corticospinal tract in the
lateral spinal cord. The rubrospinal tract influences flexor tone, particularly of
proximal arm muscles. Lesions of the nucleus are never clinically pure, as signs are
dominated by effects of damage to the superior cerebellar peduncle. The so-called
"rubral tremor" is probably due to the cerebellar outflow lesion.
D. Superior Cerebellar Peduncle
The superior cerebellar peduncle or brachium conjunctivum contain the bulk of
cerebellar outflow. Fibers cross in the prominent decussation, fan around and
through (with some fibers synapsing) the red nucleus, and then head up to ventrolateral
nucleus of thalamus. Lesions cause profound intention and postural tremor, the
laterality of which depends upon the site of the lesion relative to the decussation.
 |
Schematic of the medulla. From Afifi AK,
Bergman RA. Basic neuroscience 1986.(click on image for a larger view) |
 |
E. Lemnisci
The medial lemnisci, spinothalamic tracts,
trigeminothalamic tracts, and lateral lemnisci all converge in the dorsolateral midbrain
en route to thalamus.
F. Oculomotor (III) Nucleus
The oculomotor nucleus provides innervation to ipsilateral
inferior rectus, inferior oblique, medial rectus, contralateral superior rectus, and
bilateral levator palpebrae muscles. The Edinger-Westphal nucleus caps the IIIrd
nucleus and supplies parasympathetic pupilloconstrictor fibers and accommodation fibers to
the lens. The latter fibers cause the lens to become more round and better able to
focus on near objects. Despite the presence of crossed and uncrossed efferents from
the nucleus, the exiting IIIrd nerve innervates strictly ipsilateral muscles. A
complete oculomotor lesion causes ophthalmoplegia with retained ability only for lateral
gaze (VI) and slight downgaze (IV -- but note that IV is in a position of disadvantage
with the eye abducted), large fixed pupils, and ptosis. (What other lesion can give
ptosis?) As a mnemonic, remember, a third nerve palsy is like an intern: "down, out
and blown!"
The pupilloconstrictor fibers run on the outside of the
superior portion of IIIrd nerve. This detail becomes important in external
compressions of N. III, usually from aneurysm or herniating temporal lobe, since the
pupil will be affected before a substantial ophthalmoplegia develops. The reverse
holds true for infarcts of the IIIrd nerve, e.g., diabetic or vasculitic in which there is
relative sparing of the pupil.
In analyzing oculomotor palsies, first try to place the
deficit within the action of one oculomotor nerve. If this proves impossible, think
of more central (e.g., hemispheral gaze palsies, internuclear ophthalmoplegias) or more
peripheral (e.g., cavernous sinus lesions affecting III, IV, V1, or VI or muscle problems
from diseases such as myasthenia, thyroid disease, orbital masses or pseudotumor, and
ophthalmic myopathies).
G. Pretectum
The pretectal region (not shown) lies just rostral to the
region of the IIIrd nucleus, dorsal to the cerebral aqueduct, and just below the
pineal. In this region lies the posterior commissure and several poorly understood
nuclei. The region is clinically important for two reasons: it appears to be
concerned with upward gaze; and it is the region for mediation of the pupillary light
reflex. Certain clinical conditions (for example, neurosyphilis or a pineal tumor)
may block reaction to light but preserve accommodation-induced pupillary
constriction. This is called "light-near dissociation." The syndrome of
light-near dissociation, limited upgaze (Parinaud's syndrome), and retractory nystagmus on
attempted upgaze is strong evidence for a dorsal midbrain lesion.
H. Periaqueductal Gray
The periaqueductal gray is part of the reticular formation
activating system, although its relation to the reticular formation in pons and midbrain
is tenous. Profound coma may be caused by lesions in the periaqueductal gray,
otherwise obtainable only by widespread bilateral lesions in both cerebral hemispheres.
I. Aqueduct of Sylvius (Cerebral Aqueduct)
Along with the foramina of Monroe, Magendie, and Luschka,
this is a "bottle-neck" of the ventricular system (review the normal flow of
cerebrospinal fluid). Lesions here will cause a non-communicating hydrocephalus with
dilation of the lateral and third ventricles.
J. Colliculi
Superior colliculi are primitive processing centers for
visual information and the inferior for auditory. They are largely supplanted in
higher mammals by cortex but still play a role in orienting to light or sound and in light
reflexes.
V. CEREBELLUM
The functions of the cerebellum are not well understood,
particularly when one considers that there are more neurons in the granular cell layer
alone of the cerebellum than in the rest of the entire central nervous system (CNS).
Clinically, lesions of the cerebellum affect balance and movement.
A. Vestibulocerebellum
The vestibulocerebellum consists of the flocculonodular
lobe with connections to the vestibular nuclei and eye movement centers. Lesions in
this system (the oldest part phylogenetically) cause tilting to the side of the lesion,
gaze-evoked nystagmus (worse when looking to the side of the lesion), impaired smooth
pursuit, and downbeat nystagmus. Saccades are normal.
B. Vermis and Anterior Lobe
This portion of the cerebellum, located midline and
anteriorly, is referred to as the paleocerebellum. It governs truncal balance, leg
coordination, and saccadic eye movements. Connections are received from the
spinocerebellar tracts among other systems. Lesions lead to truncal instability when
sitting or standing, ataxia on heel-shin testing, and inability to tandem-walk.
There may be saccadic dysmetria. Alcohol toxicity predominantly affects this portion
of the cerebellum.
C. Lateral Hemispheres
Lateral hemispheres comprise the main bulk of the
cerebellum, lateral to the vermis and posterior to the primary fissure (in front of which
is the anterior lobe, grouped functionally with the midline cerebellum). This
portion is called the neocerebellum, because it matured phylogenetically with growth in
importance of upper-limb and head coordination. Lesions of this system affect
speech, face, and throat coordination and fine movements of the hands. Certain eye
movements may also depend upon the lateral hemispheres. Lesions of the hemispheres
cause ipsilateral intention tremor on finger-to-nose testing, inability to perform rapid
alternating movements ("dysdiadochokinesis"), difficulty with rhythmic motor
activities, and an abnormal modulation of the voice. Motor tone may be decreased or
unchanged. Reflexes are unaffected unless the decrease of tone allows a limb to
swing back and forth in an imitation of a pendulum -- so-called "pendular"
reflexes.
The outflow from the cerebellum is through deep nuclei
which receive afferents from the cerebellar Purkinje cells in cerebellar cortex. The
outflow nucleus for the neocerebellum is the dentate nucleus. Fibers leave the
dentate via the brachium conjunctivum, pass to and around the red nucleus after
decussation, and on up to ventrolateral nucleus of thalamus. This nucleus projects
to motor cortex. Motor cortex, in turn, projects down to the pontocerebellar system,
thereby forming a functional loop from cortex to pons to neocerebellum to dentate to
ventrolateral thalamus to motor cortex.
VI. THALAMUS
The thalamus is the relay station for all sensory and motor
system inputs to neocortex with the exception of smell. Clinical opinion holds that
certain forms of perception, e.g., pain, are mediated primarily at a thalamic level.
Thalamic nuclei are defined as primary, association, or reticular, depending upon whether
they interconnect with primary sensory or motor cortex, association cortex, or diffuse
regions of brain, respectively. The most important thalamic nuclei are listed below.
A. Ventroposterolateral and Ventroposteromedial Thalamus
(Primary)
Ventroposterolateral thalamus receives somatosensory
afferents from the body (spinothalamic tract, dorsal columns via medial lemniscus) and
relays to postcentral gyrus. Ventroposteromedial thalamus is the adjacent and
corresponding relay station for somatosensory input from the face.
B. Medial and Lateral Geniculates (Primary)
These are the relay stations for audition and vision,
respectively, to cortex in the Sylvian fissure posteriorly for audition and to medial
occipital cortex for vision. Please review the course of visual fibers from retina
to cortex with attention to field cuts produced by lesions at specific sites.
C. Ventralis Lateralis (Primary)
Ventralis lateralis is the most important motor nucleus of
thalamus, serving as a target of fibers from cerebellum, basal ganglia, and motor
cortex. It projects to the motor cortex. Despite its importance, lesions
restricted to ventralis lateralis do not cause paralysis (this only happens if lesions
extend laterally to internal capsule), and surgeons occasionally lesion ventralis
lateralis to reduce tremor associated with cerebellar or basal ganglia disease. The
nucleus ventralis anterior is partly related to ventralis lateralis and partly to the
reticular thalamic nuclei.
D. Anterior Group (Association)
The anterior group of nuclei are important relays in the
circuit of Papez, which links the limbic system (postulated to be concerned with emotions,
visceral function, and memory) to cortex. The anterior nuclei receive connections
from the fornix, which is the outflow tract of the hippocampus, and also from the
hypothalamus via the mammillothalamic tract. Anterior nuclei send afferents to
cingulate cortex. The white matter of the cingulate gathers as the cingulum bundle
and wraps around near the lateral ventricle to synapse in the cortex overlying the
hippocampus. Thus, Papez's circuit is hippocampus-fornix-anterior thalamus-cingulate
gyrus-cingulum bundle-perihippocampal cortex-hippocampus.
This is a convenient place to list the structures sometimes
classed as part of the limbic system (there is not general agreement): hippocampus,
perihippocampal cortex, olfactory association cortex, amygdala, anterior thalamus, and
cingulate cortex. Hypothalamus should probably be included, but it usually is
not. The amygdala is a deep collection of nuclei in the anterior temporal lobe,
situated just inside the bulge of the uncus. It has been said to mediate the
"four Fs: feeding, fighting, fleeing, and sex." Both amygdala and hippocampus
play prominent roles in temporal lobe seizures. A structural lesion in the region of
the uncus or adjacent orbitofrontal cortex will cause an "uncinate fit" with a
smell aura and subsequent psychomotor seizure.
E. Reticular Group of Nuclei
The reticular group of thalamic nuclei will not be named
separately, but many of them are located within lamina separating other thalamic nuclear
groups, so they may be referred to as "intralaminar" thalamus. These
nuclei are the rostral extent of the reticular formation. Stimulation with regular
pulses of electricity will cause widespread and synchronous EEG potentials in cortex.
Comment: Clinical lesions generally do not affect an
isolated nucleus of thalamus. Consideration of a thalamic problem comes up in a few
particular circumstances.
1. In a setting of a small stroke where pain and
temperature sensation are diminished, perhaps in conjunction with certain localized motor
deficits attributable to the adjacent internal capsule but where cortical function is
preserved. In this instance, an occlusion of a deep perforating branch of the
posterior cerebral may be suspected, causing a thalamic infarct.
2. Thalamic pain syndrome of Dejerine-Roussy: partial
lesions of thalamus may lead to an unpleasant and difficult-to-treat type of burning pain
in the contralateral face and body year later.
3. Massive hemorrhages may occur in the region of
thalamus. Mass effect on the pretectal region leads to paresis of upgaze and
"irritative" accommodation, so that the patient looks down at his nose.
This, plus a dense sensory deficit, will be a clue to thalamic hemorrhage.
4. As noted above, lesions may be placed in
ventrolateral intentionally to treat tremor. This was a much more common procedure
before the advent of L-dopa in treatment of parkinsonism.
VII. HYPOTHALAMUS
It is not necessary for the student to distinguish
individual hypothalamic nuclei, as the functional groups are regional in hypothalamus and
not linked to specific nuclei. As a whole, hypothalamus borders the lower part of
the third ventricle and sits just above the optic chiasm and pituitary. It is the
probably origin of autonomic and hormonal influences, and it is closely related to the
limbic system. A few regions are worth specific mention.
A. Supraoptic and Paraventricular Nuclei
These sit anteriorly in the thalamus in the region above
the optic chiasm and send neurosecretory fibers into the posterior pituitary.
Evidence suggests that the supraoptic nucleus secretes antidiuretic hormone and the
paraventricular nucleus, oxytocin. Many CNS and extra-CNS lesions can lead to a
syndrome of "inappropriate secretion of antidiuretic hormone," whereby the
kidney holds on to too much water. If the supraoptic nucleus is rendered inactive,
then the opposite condition, diabetes insipidus, occurs.
B. Anterior Hypothalamus
In addition to the nuclei listed above, the anterior
hypothalamus comprises "cooling centers" which sense elevated temperature and
direct a response of sweating and cutaneous vasodilation. Anterior hypothalamic
lesions may result in hyperthermia. A posterior center concerned with heat retention
is less certain.
C. Medial Hypothalamus
The ventromedial portion of hypothalamus is thought to
contain a "satiety" center for feeding. Lesions in this area lead to
overeating and also a condition known as "sham rage."
D. Lateral Hypothalamus
The lateral hypothalamic region appears to contain
"feeding centers." Bilateral lesions here abolish the desire to eat.
Through the lateral hypothalamus courses the medial forebrain bundle, arising from
olfactory and limbic structures and continuing down to the brainstem. Animals and
humans will work very hard to deliver stimuli to the region of the medial forebrain
bundle, whereby colloquial usage has designated this region as one of the "pleasure
centers" of the brain. In actuality, many regions are positively reinforcing,
and many others are negatively reinforcing.
E. Mammillary Bodies
These protruberances are located in the posterior
hypothalamus. Because of their deterioration in cases of Wernicke's encephalopathy
(thiamine deficiency), they have been presumed to be involved in memory.
Nonetheless, many periventricular lesions are found in Wernicke's (from medial thalamus to
periaqueductal gray and bulbar cranial nerve nuclei) besides the mammillary bodies.
The hippocampus, which is also thought to be involved in memory, projects a major
component of the fornix to the mammillary bodies. As noted above, mammillary bodies,
in turn, project the mammillothalamic tract to the anterior nuclear group for a sideloop
on the limbic circuit of Papez.
F. Hypophysial Portal System
Branches of the internal carotid artery surround the
pituitary stalk. Evidence is strong that factors with hormonal activity are secreted
by cells in hypothalamus to be transported via the portal vessels to anterior
pituitary. Hormones affected are: growth hormone; prolactin; the gonadotrophins,
luteinizing hormone and follicle-stimulating hormone; thyroid-stimulating hormone; and
adrenocorticotrophic hormone. Studies of these relations comprises the rapidly
expanding field of neuroendocrinology.
VIII. HEMISPHERES
The cerebral hemispheres comprise the cortex, subcortical
white matter, basal ganglia, thalamus, subthalamus, hypothalamus and cerebral
ventricles. The cerebral cortex reflects the highest evolutionary development of the
animal kingdom, and a correspondingly great diversity of function. Only the briefest
outline can be presented here.
Cortex can be divided into primary sensory-motor areas and
association areas. The motor cortex lies in the frontal lobe anterior to the
Rolandic (central) sulcus. Pre-motor cortex lies anterior and supplementary motor
cortex anterior and superior to pre-motor cortex. Electrical stimulation of motor
cortex produces elementary movements. The superior regions relate to leg movements,
lateral cortical areas to trunk and hand, inferior cortex to face. More anterior
stimulation produces more complex motor behaviors. Motor cortex interacts with
association cortex, ventrolateral and anterior thalamus, basal ganglia and
cerebellum. It gives rise to the corticospinal tract and extra-pyramidal movement
systems. A lesion of motor cortex lesion produces a contralateral upper motor neuron
syndrome, with disuse paralysis or slowness of fine movements, spasticity and
hyperreflexia.
Primary sensory cortices include somatosensory cortex in
parietal lobe, posterior to the Rolandic sulcus. There is a sensory representation
parallel to the motor homunculus, with leg superior and face inferior. Lesions here
produce loss of discriminative sensation: textures, 2-point discrimination, joint
position, graphesthesia (Vibration and crude touch sensation may be mediated
thalamically).
Visual cortex includes the occipital tip and medial occiput
along the banks of the lingual gyrus. The input to this system arises in the retina,
half crosses in the optic chiasm, then fibers travel to the lateral geniculate nucleus of
thalamus, and to the occipital cortex.
Fiber collaterals are given off to the superior colliculus
in midbrain to mediate the pupillary reflexes. Several different patterns of visual
system lesions are important for lesion localization. Two rules are important to
understand the system. First, visual field lesions (scotoma) are always localized
with respect to the patient's perspective. A left superior scotoma means the patient
cannot see clearly up and to his or her left. Second, the lens inverts up to down
and left to right. A right inferior retinal lesion thus produces a left superior
field cut. A retinal lesion (e.g., retinal hemorrhage or infarction) produces an
irregular scotoma in the visual field of one eye. Lesions of fibers after crossing
in the chiasm produce homonymous field deficits (similar shape in both visual
fields). Total destruction of the right occipital pole would produce a left
homonymous hemianopsia. Due to embryological growth of the temporal lobe laterally,
the fibers (called Meyer's loop) from inferior retina sweep laterally into the posterior
temporal lobe. Superior retinal fibers take a straighter course through parietal
white matter. Lesions of the right posterior temporal lobe may therefore involve
only those fibers from the left inferior retina, which see the right visual field.
This will produce a right superior quadrantinopsia, mnemonically recalled as
"pie-in-the-sky." Discovery of pie-in-the-sky visual field cuts should mandate a
search for a contralateral posterior temporal lobe lesion. Pituitary adenomas or
craniopharyngiomas are midline tumors that may impinge directly on the optic chiasm.
This destroys the decussating fibers from medial retinas (temporal fields).
Bi-temporal heteronomous hemianopsias result, i.e., patient can not see past either
midline laterally.
Auditory deficits are rarely produced from cortical
lesions, since the auditory inputs are highly crossed and bilateral. Fibers travel
from the cochlea via the VIIIth nerve to the dorsal and ventral cochlear nuclei in the
pons, then to the superior olive and trapezoid body. Fibers here ascend crossed and
uncrossed to the medial geniculate body (with collaterals to the inferior colliculus) and
then to auditory cortex (Heschel's gyrus) in the posterior bank of the Sylvian fissure.
Olfactory bulb connects to ipsilateral olfactory tract to
olfactory stria on the undersurface of the frontal lobe. These have clinical
significance in at least 3 areas. Olfactory lesions (anosmia) will diminish the
sense of taste, and sometimes give clues to the presence of a sphenoid ridge lesion, such
as a meningioma. Secondly, olfactory cortex in frontal lobe has strong connections
to medial inferior temporal structures, including the amygdala. This is a key
structure (along with hippocampus) for temporal lobe seizures. A stereotyped bad
smell may be a warning of an impending temporal lobe seizure. Third, structures in
the region of olfactory cortex include the nucleus of the diagonal band and the nucleus
basalis of Meynert. These regions provide much of the cholinergic input to
forebrain, and appear deficient in people with Alzheimer's Disease.
Functions of frontal and parietal association areas are
poorly understood. The frontal association area is involved in sequencing behavior
in time: one over-simplification would be to think of this area as a "delayed
gratification" center. People with frontal lobe lesions have difficulty
planning for the future and inhibiting expression of immediate needs. Parietal
association regions integrate numerous sensory and motor functions. Parietal lesions
produce deficits of attention, spatial construction, appreciation of part-whole
relationships. A variety of agnosias ("not knowing") and apraxias
("not performing") result from parietal lesions.
In clinical practice a major fraction of cortical lesions
result from stroke. Three main vessels supply cortex: anterior, middle and posterior
cerebral arteries. Infarction in the territory of the anterior cerebral produces
frontal lobe signs and weakness greater in leg than arm or face. Middle cerebral
artery infarcts produce contralateral hemiparesis, greatest in hand and face. If the
stroke is on the speech dominant side there will also be aphasia. Posterior cerebral
infarcts produce visual deficits and mesial temporal infarcts, which may impair memory.
