Nincs diacm

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The brain stem
The cranial nerve nuclei and nerve fascicles and
the long ascending and descending neural tracts
are closely juxtaposed in the brain stem.
Therefore, lesions in the brain stem typically
damage both segmental (cranial nerve) and
inter-segmental (long tract) structures, leading
to characteristic combinations of neurologic
deficits. A common syndrome with brain stem
lesions is one or more cranial nerve palsies
ipsilateral to the lesion associated with
contralateral long-tract deficits. This
presentation occurs because most cranial nerves
innervate ipsilateral structures, whereas the
long tracts decussate at or below the level of
the caudal medulla.
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The mesencephalon (midbrain) 1.The tectum
quadrigeminal plate inferior colliculi relay
station for the lateral lemniscus (auditory
pathway) - medial geniculate body- auditory cx
superior colliculi optic stimuli from the
retina and occip. cx., auditory stimuli from
the inf. coll., fibers from the spinal cord.
Turning the head in the direction of noise,
sudden visual stimuli. Automatic pursuit
movements. Vertical gaze (Parinaud
syndrome) 2.The tegmentumbetween the subst.
nigra and the tectum, red nucleus
(rubrospinal and rubroreticular tracts).
Control of posture, muscle tone. N. III.
IV., Edinger-Westphal and Perlia nuclei 3.The
substantia nigra Parkinsons disease 4.The
cerebral peduncles or crura cerebri.
Cortico-nuclear, cortico-spinal and
cortico-pontine fibers
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The pons 1. Basis pontis nuclei pontis (relay
for the cortico-ponto-cerebellar pathway 2.
Tegmentum pontis V.,VI.,VII., VIII cranial
nervenuclei 3. Superior, middle and inferior
cerebellar peduncles The medulla oblongata 1.
Pyramids 2. Inferior olivary nuclei
(olivocerebellar tract, controls precision of
voluntary movements) 3. IX., X., XI., XII.
cranial nerve nuclei
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The ascending and descending pathways 1.
Cortico-spinal, cortico-nuclear,
cortico-ponto-cerebellar 2. Medial longitudinal
fasciculus (from teh mesencephalon to the spinal
cord) interconnects the nuclei of the ocular
nerves, cervical spinal cord (neck muscles), the
vestibular nerves, reticular formation (gaze
centers), basal ganglia, cerebral cortex 3.
Olivo-cerebellar tract controls precision of
movement 4. Anterior and posterior
spino-cerebellar tracts impulses related to the
movement (somatosensory and segmental
interneurons) 5. Tr. spinalis et mesencephalicus
n.V. sensory impulses from the face and masseter
reflex. 6. Lateral lemniscus fibers from the
cochlear nuclei through the trapezoid body to the
inferior colliculi. 7. Spinothalamic tract,
medial lemniscus
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Wernicke's encephalopathy Thiamine deficiency,
most frequently in alcoholic patients (or
malnutrition). Multiple focal lesions in the
thalamus, mammillary bodies, superior cerebellar
vermis, periaqueductal gray matter, pons and
medulla near the floor of the fourth ventricle.
The abducens, medial vestibular, and dorsal
motor vagus nuclei are damaged. Classic clinical
presentation a triad of global confusional
state, truncal ataxia and ocular signs (bilateral
abducens nerve palsy, internuclear
ophthalmoplegia, conjugate gaze paresis,
spontaneous or gaze-evoked nystagmus.) Advanced
disease may cause complete external
ophthalmoplegia and fixed, miotic
pupils. Thiamine replacement leads to a rapid
resolution of the ocular motor abnormalities. The
ataxia resolves more slowly. The global
confusional state may evolve into the amnestic
disorder typical of Korsakoff's syndrome.
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Central pontine myelinolysis Rare disorder that
occurs most frequently in alcoholic patients and
others with debilitating diseases, such as
cancer, hepatic failure, or sepsis. Caused by
severe electrolyte disturbance (rapid correction
of hyponatremia). The myelin sheaths in the basis
pontis are destroyed, with relative sparing of
axons and cell bodies. Clinically quadriplegia
and pharyngeal paralysis that develops over a
period of several days, and it often results in
locked-in syndrome. Conjugate gaze palsies,
nystagmus, and miosis occur if the the lesion
extends into the tegmentum of the pons. Therapy
is limited to supportive care.
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Progressive bulbar palsy Motor neuron disease
in which deficits are restricted to or begin with
bulbar dysfunction. Slurred speech, change in
timbre of the voice and, later, difficulty with
swallowing. If the lower motor neuron is
involved, atrophy and fasciculations of the
tongue as well as diminished elevation of the
soft palate occur. Progressive upper motor
neuron involvement leads to diminished facial
expression, with hyperactive jaw jerk, frontal
release signs, hyperactive gag response, and
clumsiness of tongue movement without atrophy.
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The Arnold-Chiari malformation Congenital
disorder with four variants. Type II elongation
and downward herniation of the caudal medulla,
cerebellar tonsils, associated with lumbosacral
meningomyelocele, syringomyelia and
hydrocephalus. Type I malformations are similar
to type 2, but less severe and rarely associated
with spinal dysraphism. Type III
meningomyelocele in the occipitocervical region
with cerebellar herniation. Type IV cerebellar
hypoplasia Increased intracranial pressure
(headache, neck pain, nausea, and papilledema),
lower cranial nerve dysfunction, progressive
cerebellar ataxia, dementia, incontinentia,
reduction in dorsal column function, syncope,
vestibular and oculomotor dysfunction.
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Horner syndrome Parinaud syndrome
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Bulbar palsy Damage of the bulbar cranial nerves
and/or motor nuclei, and/or intramedullary fibers
and/or lowe cranial nerves. Signs paresis,
atrophy, fasciculation, diminished reflexes
Pseudobulbar (suprabulbar) palsy Bilateral
damage of the corticobulbar tract, producing
bulbar dysfunction (dysarthria, dysphagia,
paresis of the tongue) without signs of lower
motor neuron disorder. It is usually caused by
ischemic disease bilaterally in the
hemispheres(frontal white matter or inernal
capsule) or in the brain stem (basis pontis).
Multiple lacunar infarcts may result in some
combination of pseudobulbar palsy, gait ataxia,
subcortical dementia, and incontinence (like in
Binswanger's disease).
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Listeria rhombencephalitis a focal infection by
Listeria monocyt. Multiple abscesses in the pons
and medulla. Fever, headache, and nausea,
followed by multiple cranial nerve palsies,
long-tract signs, and obtundation. Ampicillin and
gentamicin is the preferred therapy. Whipple's
disease caused by a bacilliform bacteria.
Non-neurologic symptoms weight loss, abdominal
pain,diarrhea, arthralgia, fever. Neurologic
signs cognitive dysfunction, myoclonus, ataxia,
somnolence, lowing of vertical saccadic eye
movements,restriction of vertical and horizontal
gaze. Oculomasticatory myorhythmia (pendular
vergence oscillations of the eyes associated with
concurrent contraction of the masticatory
muscles). Brain stem gliomas astrocytomas in
the pons which diffusely infiltrate the brain
stem. Most common in children and young adults.
Combination of cranial nerve palsies, cerebellar
and pyramidal signs. Hydrocephalus (if the fourth
ventricle is obstructed).
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The reticular formation Prevades the tegmentum
of the entire brain stem. The medial column is
the effector portion of RF (Gigantocellular,
Ventral reticular, Pontine reticular
nuclei) Large neurons with extensive dendritic
arbor, long ascending and descending axons,
numerous collat. Target structuresother regions
of the RF, cranial nerve nuclei interlaminar
nuclei of the thalamus,spinal cord The lateral
column is the afferent portion of RF
(Parvocellular, Parabrachial, Pedunculo-pontine
nuclei) Small neurons, numerous collaterals from
the sensory tracts (spinothalamic,
trigeminothalamic, auditory), and direct input
from spinoreticular tracts. Raphe nuclei
serotonergic system Red nucleus rubrospinal,
rubroreticular pathways Periaqueductal gray
matter integrates the autonom, limbic and
nociceptive stimuli. Reciprocal innervation
hypothalamus, frontal cx., ascending,limbic
system, other RF structures, sensory tracts
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The monoaminerg systems of the RF Noradrenerg
Locus ceruleus connections with the spinal
cord, thalamus, hippocampus, and
cerebral cortex Lateral tegmental neurons
integrates autonomic functions
(connection to the sympathetic
pregangl.neurons, solitary tract, dorsal motor
vagus nucleus. Stimulation causes
dramatic decrease of pulse rate and
blood pressure. Dopaminerg Mesostriatal
system subst. nigra/striatum control of
voluntary movement (Parkinsons disease)
Mesolimbic and mesocortical system from the
ventral tegmentum, take part in
cognitive processes Serotonerg Raphe
nuclei descending fibers to the spinal cord
increases the excitability of motor neurons,
modulates pain sensation
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1. Arousal Consciousness a person's ability to
be aware of self and the environment and to
orient toward new stimuli. ARAS (Moruzzi and
Magoun 1949) Ascending sensory tracts -
Lateral column of RF - Medial column of RF -
Central tegmental tract - hypothalamus and
intralaminar thalamus nuclei - Thalamocortical
fibres - Cortex and subcortical
structures 2. Sleep-wakefulness cycle 3. Pain
transmission Ascending sensory tracts -
Lateral column of RF - Serotoninergic raphe
neurons - Reticulobulbar and spinal tracts-
Dorsal horn neurons serotonin inhibits
pain transmission (enkephaline) Stimulation
of periaqueductal gray induces analgesia
(opiate mechanisms).
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4. Regulation of muscle tone, deep reflexes, body
posture Pontine efferents (reticulo-spinal tr.)
enhances extensor tone Medullary efferents
inhibit extensors, enhances flexor tone 5.
Integration of conjugate eye movements
Paramedian pontine reticular formation
integrates horizontal eye movements.
Efferents sup. colliculus, vestibular nu., RF,
frontal eye field Afferents ipsilateral VI.
nu., MLF,contralateral III.nu. 6. Vital visceral
responses Visceral sensory input to RF (from
asc. sensory, nu. tr. solitarius, hypothalamus,
limbic system) Cardiovascular Cardiac rhythm
and blood pressure are diminished after
stimulation of raphe nuclei. Respiratory
rhythm Inspiration gigantocellular,
exspiration parvicellular nucleus.
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Thalamus Diencephalon Thalamus, subthalamus,
epithalamus, hypothalamus Functions of the
thalamus I. Relay functions from the spinal
cord, brainstem, cerebellum basal ggl. to the
cortex II. Modulatory functions Influences the
excitability of the cx, synchronised vs.
desynchronised states (repetitive and burst
firing) III. Integrative functions 1. Sensory
connections (sensory relay station) 2. Motor
coordination 3. Psychological functions
(instinct, affection, limbic functions etc) 4.
Autonom function control 5. Cortical activation
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Blood supply of the thalamus Individual
variability 1. Tuberothalamic a. (from posterior
commun. a.) anteroventral-medial nu. 2.
Paramedian vessels (from basilar artery)
ventromedial nuclei 3. Inferolateral artery (from
posterior cerebral a.) ventrolateral nuclei 4.
Posterior chorioid a. (from posterior cerebral
a.) anterior nuclei
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The motor thalamus Nuclei of the anterolateral
reion Afferentation Nuclei
Efferentation subst. nigr VA, VM, SMA, area
6, prefron.cx pallidum ansa leticul. VA,
VL area 6, area 4, fasc. lenticul. SMA cere
bellothalamic VLp area 4, area 6,
connections SMA Paralel
projections
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Somatosensory thalamus Afferentation Nuclei
Efferentation Med. lemniscus VP pr.
sensory cx. Spino-trigemino-thal. topographic
sec. sensory cx. Spino-cervico-thal. organisat
ion (lamina Vth.) Taste- nucl.solitary
tract VPM insular,
opercular cx., pr. sensory
cx.
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Lesion of the paramedian region Various clinical
signs due to reciprocal connections with
cortical (prefrontal, limbic, paralimbic) and
subcortical (brainstem, hypothal., basal ggl,
basal forebrain, tectum, spinal cord)
structures. VMP motor thalamus motor
signs MD ARAS disturbed consciousness Reticul
ar nucleus ARAS disturbed consciousness Intrala
m. synch.-desynch. sleep disturbance Nucleus cort
ical activity cerebellum LGN gaze
disturbance Cajal nu. oculomot.nucl. ptosis,
mydriasis Anter.nucl. thalamo-frontal thalamus
dementia, memory dist., thalamo-limbic emotiona
l lability, irritability, agression,apathy,
disturbed abstract thinking
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Dejerine-Roussy syndrome (1906) Caused by the
vascular lesion of the somatosensory thalamus
(ventrolateral posterior nuclei) 1. Hemiparesis
deafferentation of the motor cortex
internal capsule 2. Hemihypaesthesia,
astereognosis 3. Hemiataxia crossed
cerebellar diaschisis 4. Involuntary movements,
dystonia nigro-thalamic,
thalamo-striatal connections 5. Thalamus pain
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Lesion of the anterolateral region Right
thalamus hemineglect, asomatognosia,
constructive apraxia,apathy.Thalamus
neglect due to disturbed attention and
vigilance (cortico-limbic-reticular
connect.) Left thalamus thalamus aphasia
transcortical-like, paraphasias, perseveration,
decreased spontaneous speech, low
volume Thalamus pain Hyperpathy (spontaneous,
non-painful stimulus evokes it) Lesion VPM, VPL
(not known pathomechanism) Starts with latency
(days or weeks). Usually transient. Thalamus and
epilepsy The thalamus itself is not capable to
generate epileptic activity, however plays
important role in generalization of
seizures. Absence epilepsy 3 Hz spike-and-wave
activity Sleep-wakefulnes cycle ----- epilepsy
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