1. health and fitness
2. disease

Clinical Connections
Clinical Connection: Spina
Bifida
• Defective closure of the caudal
neural tube
• Variabilility in severity
– Spina
– Spina
– Spina
– Spina
– Spina
bifida
bifida
bifida
bifida
bifida
oculta
cystica
with myelomeningocele
with meningomyelocele
with myeloschisis
Clinical Connection: Spina
Bifida
• Often occurs with other congenital
anomalies
• Incidence declining with early
prenatal detection and dietary
supplement of folic acid
Image spina bifida
Clinical Connection:
Arnold-Chiari Malformation
• Associated often with spina bifida
with meningomyelocele
• Congenital anomaly
• Medulla and posterior cerebellum
elongate into foramen magnum
• May be asymptomatic
• May result in hydrocephalus and
other symptoms
Clinical Connection:
Anencephaly
• Congenital anomaly
• Failure of rostral neuropore closure
• Large portions of scalp, cranial
bones, and cerebral hemispheres are
absent
• Most die in utero, virtually all by first
postnatal week
Clinical Application Exercise
• Discuss the stories of Maria Rodriquez and Jonathan
Perry
• Mechanism of injury
• For Maria, do you predict motor loss, sensory loss
or both? Why? Both, Ant/post
• Predict her ‘motor picture’ mid trunk & up
• Will she walk? No
• For Jonathan, which part of the cord has the tumor
affected? Posterior
Clinical Connection: Nervous
System Pathology
• Retrograde transport of certain
toxins and viruses from the
environment to the CNS
• Examples
– Clostridium tetani bacterium
– Rabies
– Herpes simplex virus
– Poliomyelitis
Clinical Connection:
Multiple Sclerosis
• Autoimmune disorder
• Proteins expressed by
oligodendrocytes are erroneously
recognized as foreign by immune
system
• Loss of myelin in brain and spinal
cord
Clinical Connection:
Parkinson's Disease (PD)
• In PD there is a degeneration of
dopamine (DA) producing cells and
a substantial reduction in the
synthesis of DA
• Most common treatment strategy is
replacement therapy of DA
Clinical Connection:
Parkinson's Disease (PD)
• DA cannot cross blood–brain barrier,
but precursor L-DOPA does
• L-DOPA stimulates surviving DA cells
to increase synthesis of DA
Clinical Connection:
Biologic Depression
• May be due to a deficiency in brain of
amine transmitters – norepinephrine
(NE) and serotonin (5-HT)
• Monoamine oxidase is an enzyme
that breaks done NE and 5-HT
• Treatment historically included MAO
inhibitors
• MAO inhibitors have unwanted side
effects
Clinical Connection:
Syndrome of the Anterior Spinal
Artery
• Usually acute onset due to
ischemia of lower thoracic or
upper lumbar spinal cord
Clinical Connection:
Syndrome of the Anterior Spinal
Artery
• Characterized initially by
– Flaccid paraplegia in both legs
– Bilateral deficits in STT sensibilities
– Loss of bowel and bladder control
– Sparing of DCML sensibilities
• Following spinal shock, spastic
paraplegia may develop
Clinical Connection:
Herniation of the Vertebral
Disc
• Displacement of disc tissue from
normal position between vertebral
bodies
– Nuclear protrusion mild
– Disc prolapse more severe
Disc Herniations
Clinical Connection:
Herniation of the Vertebral
Disc
• May compress the spinal cord against
the vertebral canal of the spinal nerves
against the intervertebral foramina
• Most herniations are in a posterolateral
direction
• Common levels for herniations
correspond to areas where vertebral
column moves freest
– L5/S1, C5/C6, C6/C7
Clinical Connection: Vertebral
Fractures and Neurotoxic Spinal Cord
Injury
• With vertebral dislocations or
fracture dislocations the spinal cord
can be damaged immediately by
trauma or subsequently through
secondary neurochemical injury
• Endogenous neurotransmitters cause
excitotoxic neuronal cell death
• Initial trauma causes changes in ions
leading to cytotoxic edema
Clinical Connection: Cervical
Spondylosis
• Degeneration of the discs and
surrounding ligaments, osteophytic
changes
• Lower cervical vertebra particularly
vulnerable
Clinical Connection: Cervical
Spondylosis
• Results in compression and
compromised blood supply of spinal
cord
• Characterized by neck pain and
stiffness, hand numbness, and spastic
leg weakness
Spondylosis
Clinical Connection:
Control of the Level of Consciousness
• The portion of the RF that
contributes to the level of
consciousness is called the ascending
reticular activating system (ARAS)
• Sleep is a part of this, epithalamus is
main contributor of cycles
(melatonin)
Clinical Connection:
Control of the Level of Consciousness
• Levels of consciousness
– Attention
– Alertness
– Drowsiness
– Stupor
– Coma
Clinical Connection: Thalamic
Syndrome
• Typically caused by occlusion of
thalamogeniculate branches of the
PCA supplying posterior thalamus
• Symptoms contralateral to lesion
– Hemianesthesia, ataxia, excruciating
neurogenic pain
Symptoms in diff proportions in diff pts
• Unresponsive to analgesics
Clinical Connection:
Hypothalamic Syndromes
• Diabetes INSIPIDUS
• Problems with regulation of thirst,
hunger, and body temperature;
menstrual and sleep–wakefulness
cycles
Clinical Connection:
Cerebellar Dysfunction
• Variety of causes
– Acute/chronic alcohol intoxication,
developmental disorders, stroke, trauma
• Characteristic symptoms
– Hypotonia, incoordination, intention
tremor, ataxia, nystagmus
Clinical Connection: Involuntary Movements
Attributed to Basal Ganglia Dysfunction
• Tremor-rhythmic, alternating
movement of a body part
• Athetosis – slow, sinuous, writhing
movements
• Chorea – brisk, graceful, complex
movements (caudate)
• Ballismus – forceful, flinging
movements (subthalamic)
Clinical Connection: Occlusion
of the MCA
• Occlusion of the superior division of
the MCA
– Structures affected: BAs 4, 3, 1, 2, 8,
44, 45
– Related symptoms include contralateral
motor and sensory deficits, eye
movement deficits, and motor aphasia if
dominant hemisphere occluded
– Problem with language production
Clinical Connection: Occlusion
of the MCA
• Occlusion of the inferior division of
the MCA
– Structures affected: BAs 22, 39, 40
– Related symptoms include sensory
aphasia if dominant hemisphere
occluded, visuospatial deficits if
nondominant hemisphere occluded
infarcted by occlusion of the
left superior division of the
MCA. Note that the damage is
confined to the frontal lobe and
postcentral gyrus of the
parietal lobe. (b) Area of the
left hemisphere infarcted by
occlusion of the inferior division
of the MCA. Note that the
damage is confined to the
posterior portion of the parietal
Clinical Connection: Occlusion
of the ACA
• Less common than occlusion of the
MCA or IC
• Structures damaged include the medial
aspects of BA 4, 3, 1, 2
• Related symptoms include contralateral
motor and sensory deficits that are
most severe in the lower extremity
Occlusion of the ACA
Clinical Connection: Occlusion
of the IC
• Carotid border syndrome occurs with
occlusion of 70% or more of the IC
• Blood flow to the distal territories is
decreased, but not eliminated
• Symptoms include contralateral
numbness and weakness
Clinical Connection: Occlusion
of the PCA
• Structures affected include BA 17,
the primary visual cortex
• Related symptoms include loss of
vision in the contralateral one-half of
the visual field of each eye
• Because a branch of MCA perfuses
the cortex that receives afferents
from the fovea, there may be sparing
of foveal vision (macular sparing)
Clinical Connection: Motor
Signs
• Positive signs (release phenomena)
– An excess of neural activity
– Hyperreflexia, hypertonicity, Babinski sign
• Negative signs
– Motor deficits due to the loss of function
of damaged neural structures
– Weakness, loss of speed of movement,
loss of dexterity
Clinical Connections
• Peripheral neuropathies typically
impair somatosensation and
autonomic functions
• Herpes zoster (shingles) is a viral
infection of the somatosensory
ganglia of the peripheral and cranial
nerves (ophthalamic
Clinical Connections: Disorders
of Peripheral Nerves
• Neuropathy – disease of the
peripheral nerves
– Mononeuropathy – affecting one nerve
– Polyneuropathy – affecting many nerves
– Radiculopathy – affecting spinal nerve
roots
Clinical Connections: Disorders
of Peripheral Nerves
• Diabetes mellitus (DM) is the most
common cause of polyneuropathy
– Characterized by distal, bilateral sensory
losses
Clinical Connection:
Brown-Sequard Syndrome
• Lesion of one-half of the spinal cord
and all fibers entering the cord via
the dorsal root producing
– Ipsilateral zone of somatosensory
anesthesia at the damaged dermatomes
– Ipsilateral loss of DC-ML modalities
below the lesion
– Contralateral loss of STT modalities
below the lesion
Clinical Connection:
Syringomyelia
• Disease process in the center of the
spinal cord, usually over a few
cervical segments
• Disrupts pain and temperature fibers
of the STT in the ventral white
commissure
• Characterized by bilateral loss or
pain and temperature sensibility,
usually in the hands and arms
Clinical Connection:
Subacute Combined
Degeneration
• Disorder that typically first involves
the fibers of the dorsal columns
• Related to lack of Vitamin B12
absorption
• Early symptoms include symmetrical
parathesias of fingers and toes and
loss of proprioception
• Person may demonstrate unsteady,
ataxic gait
Clinical Connection: LMN
Syndrome
• Damage to the LMN cell body or axon
• Characterized by:
– Hyporeflexia
– Hypotonia
– Paralysis (loss) or paresis (weakness)
– Atrophy = rapid and severe
– Denervation
• Fasciculations = can happen in tired, healthy
people or LMN damage = visible twitch
• Fibrillations = similar to fasciculation, smaller,
need EMG, not visible twitch
Clinical Connection:
Diseases of the Motor Unit
• Four sites of the motor unit can be
attacked by specific disease entities
– The cell body of the LMN, its axon, the
neuromuscular junction, or the muscle
fibers
• Neurogenic-affecting cell body or axons
– (e.g., polio, neuropathies)
• Myopathic-affecting striated muscle
– (e.g., myasthenia gravis)
Clinical Connection: Polio
• Viral infection, prevented by
vaccination
• Attacks cell bodies of LMNs
• Cardinal clinical signs:
weakness/paralysis, atrophy, and
decreased reflexes
• Postpolio syndrome may appear 20–
30 years after the acute infection
– Remaining neurons overworked after
normal neuron apoptosis
Clinical Connection:
Neuropathies
• Pathological changes of the
peripheral nerves
– Segmental degeneration
– Axonal degeneration
– Wallerian degeneration
• Diabetes mellitus (DM)
• Acute inflammatory demyelinating
polyneuropathy (AIDP) = aka
guillanne barre’s
Clinical Connection:
Myasthenia Gravis
• Autoimmune disorder of neuromuscular
transmission resulting in weakness
• Typically eye muscles are affected first,
resulting in ptosis and diplopia
• Muscles of facial expression,
mastication, swallowing, and speech
are typically affected next, resulting in
altered facial expression, dysphagia,
and dysarthria
Clinical Connection:
Myopathies
• Progressive hereditary diseases of
skeletal muscle
• Duchenne muscular dystrophy
– Defective gene that codes for protein
dystrophin
– Sex-linked recessive trait transmitted
from mother to male children
Clinical Connection:
Myopathies
• Duchenne muscular dystrophy
– Lack of dystrophin renders sarcolemma
vulnerable
– Weakness, tearing, and loss of muscle
fibers
– Shortens life expectancy to late
adolescence or early adulthood
Duchenne Muscular Dystrophy
Clinical Connection:
Amyotrophic Lateral Sclerosis
• Also called Lou Gehrig's disease
• Most frequent motor system disease
• Characterized by
– amyotrophy (weakness, denervation,
atrophy)
– lateral sclerosis (upper motor neuron
signs)
Clinical Connection:
Amyotrophic Lateral Sclerosis
• Relentlessly progressive
• Some 50% of cases progress to
death within 2–3 years of diagnosis
• Role of the DPT
Clinical Connection: Evaluation
of Reflexes
• Is the reflex present?
• If present, is status altered (grading)?
– Hyporeflexia
– Hyperreflexia
• Are pathological reflexes present?
– Babinski or stepping response in adults
(normal in infants)
Clinical Connection: Knee
Stability
• Anterior cruciate ligament (ACL)
prevents femur from sliding
posteriorly on the tibia, preventing
hyperextension of the knee
• The hamstring muscles play a critical
role in knee stability by protecting
the ACL
Clinical Connection: Knee
Stability
• If knee moderately hyperextended,
hamstring stretch reflexes will cause
contraction of the hamstrings and
relieve the strain on the ACL
• Two phases SLR and MLR
• MLR latency associated with ‘giving
way’ in patients post ACL rupture
and surgical repair
Spasticity
• Motor disorder characterized by a
velocity-dependent increase in tonic
stretch reflexes (muscle tone) and
exaggerated tendon jerks
• Spasticity often develops in clinical
disorders with UMN damage such as
stroke, multiple sclerosis, and spinal
cord injury
Spinal Shock and the
Emergence of Spasticity
• Spinal shock – following complete
spinal cord transection or
compression, the initial response is
one of transient hypotonia and
hyporeflexia
– All sensation below the lesion is lost
– All voluntary movement below the lesion
is lost
– Reflex activity below lesion is lost
Spinal Shock and the
Emergence of Spasticity
• In addition to motor and sensory
losses, bowel and bladder function
are lost, leading to fecal and urinary
incontinence
Emergence of Spasticity
• After the period of spinal shock, the
intrinsic spinal cord circuits may
begin to display autonomous activity
• Minimal reflex activity and initially
weak flexor responses to painful
stimuli
– Mass reflex, triple flexion
Emergence of Spasticity
• Eventually and gradually, extensor
tone also increases
• Due to altered suprasegmental
influences
Triple Flexion Reflex
Pattern of Involvement of Muscles
Weakness of LMN versus UMN Damage
• LMN damage
– Flaccid paralysis or flaccid paresis of
individual muscles or groups of muscles
– Ipsilateral to the lesion
Pattern of Involvement of Muscles
Weakness of LMN versus UMN Damage
• UMN damage
– Spastic paresis of synergistic muscle
groups
– Contralateral to lesion if damage is
rostral to decussation
– Ipsilateral to lesion if damage is caudal
to the decussation
Clinical Connection:
Pathological Reflexes
• Babinski
• Flexion
• Clasp-knife
• Clonus
Clinical Connection:
Babinski Reflex
• Elicited in healthy babies as a bilateral
plantar response during first year of life
• When elicited beyond infancy, is a
reliable sign of corticospinal tract
damage
• Elicited by stroking sole of foot
• Abnormal response is dorsiflexion of
the great toe and abduction of the
other toes
Figure 11-16
(a) The normal response to stroking the sole of the foot. (b)
The abnormal Babinski sign.
Clinical Connection: Flexion
Reflex
• Flexion reflex normally elicited with
noxious stimuli
• Following UMN damage, the flexion
response may be seen with
innocuous stimuli
• Due to disruption of descending
suprasegmental inhibition
Clinical Connection:
Clasp-Knife Phenomenon
• Sometimes accompanies spasticity
following UMN damage
• Elicited with passive movement of a
limb
Clinical Connection:
Clasp-knife Phenomenon
• Limb moves freely for a short
distance, followed by a rapid
increase in resistance, followed by a
sudden giving way to movement
• Reflects the length dependence of
hyperreflexia
Clinical Connection: Clonus
• A clinical sign of spasticity
• Elicited with abrupt and sustained
ankle dorsiflexion
• Series of rhythmic involuntary
muscle contractions
Figure 11-18 Ankle clonus in an individual with spasticity consists
of rhythmic contraction–relaxation cycles of the ankle extensor
muscles (plantar flexors of the foot) in response to their sustained
stretch (i.e., stretch of the Achilles tendon).
Clinical Connection:
Combined Sensory and Motor Damage
• Brown-Sequard syndrome or spinal
cord hemisection
• Syringomyelia
• Subacute combined degeneration
Clinical Connection:
Brown-Sequard Syndrome
• Rarely encountered lesion involving
only one-half of the spinal cord
Clinical Connection:
Brown-Sequard Syndrome
• Characterized by
– Ipsilateral flaccid paralysis at the level
of lesion
– Ipsilateral spastic paralysis below the
level of lesion
– Ipsilateral loss of DCML sensibilities
below the level of lesion
– Contralateral losses of STT sensibilities
below the level of lesion
Figure 11-19 The Brown-Sequard syndrome results from injury to one-half
of the spinal cord, extending over several spinal cord segments (shaded). (a)
Degeneration (broken lines) associated with spinal cord hemisection. The
ventral white commissure is represented as a tube to illustrate the oblique
crossing of spinothalamic tract afferents before they enter the anterolateral
funiculus on the opposite side of the cord.
Figure 11-19 The Brown-Sequard syndrome results from injury to one-half
of the spinal cord, extending over several spinal cord segments (shaded). (b)
Motor and somatosensory losses associated with the Brown-Sequard
syndrome.
Clinical Connection:
Syringomyelia
• Rare and chronic disorder
characterized by a progressive
development of fluid-filled cavity in
the spinal cord, most commonly in
lower cervical or upper thoracic
regions
Clinical Connection:
Syringomyelia
• Typically a slow progression
beginning with interruption of pain
and temperature fibers crossing in
the ventral white commissure
• Hallmark symptom bilateral loss of
pain and thermal sensation
• Occasionally cavity extends rostrally
into brainstem, resulting in
syringobulbia
Figure 11-20 The cavity in syringomyelia often interrupts
spinothalamic afferents crossing in the ventral white commissure.
Clinical Connection:
Subacute Combined Degeneration
• Pernicous anemia results from an
inability to absorb vitamin B12
• Unclear mechanisms lead to
degeneration of peripheral and optic
nerves, brain, and spinal cord
• Spinal cord is the first and most
commonly affected region
Clinical Connection:
Subacute Combined Degeneration
• Posterior and lateral funiculi
degeneration is characteristic,
leading to symmetrical parathesias,
loss of dorsal column sensation, and
ataxia
• Progresses to lateral column signs of
loss of strength and UMN signs
Figure 11-21 Myelin stained sections from the lower cervical spinal cord.
(a) Normal. (b) Lesions in subacute combined degeneration involve
degeneration of the white matter in the posterior and lateral funiculi of the
spinal cord. The degenerated fibers lose their myelin and, hence, are
unstained.
Clinical Connections:
Primary Orthostatic Hypotension
• In primary orthostatic hypotension
blood pressure falls suddenly upon
standing from a recumbent position
• May be due to degeneration of
postganglionic sympathetic fibers and
sparing of parasympathetic fibers or
degeneration of the intermediolateral
cell column of the thoracic cord
Clinical Connections:
Primary Orthostatic
Hypotension
• Many other possible causes and
conditions that cause low blood
pressure
Clinical Connections:
Bladder Dysfunction
• Interruption of reflex connections of
the bladder produces neurogenic
bladder
• Reflex neurogenic bladder caused by
bilateral spinal cord lesion above
T12, resulting in UMN paralysis,
spasticity, and sudden and reflexive
emptying
Clinical Connections:
Bladder Dysfunction
• Nonreflex neurogenic bladder caused
by bilateral lesion of sacral spinal
cord, resulting in LMN paralysis,
flaccidity, and bladder leakage
Clinical Connections:
Horner's Syndrome
• Combination of symptoms:
– Miosis- small pupil
– Ptosis- drooping eyelid
– Enopthalmos (apparent) - retraction of
eyeball
Clinical Connections:
Horner's Syndrome
• Occurs as a result of lesion to
preganglionic sympathetic fibers
emerging from T1 and T2
– Causative peripheral lesions include
tumor of superior cervical ganglion,
cervical lymph lodes, and surgical
trauma to sympathetic chain
– Causative central lesions include tumor
or stroke of the brainstem, and
syringobulbia
Horner’s Syndrome
Clinical Connections:
Acute Autonomic Paralysis
• Complete lesion of the cervical spinal
cord interrupts all suprasegmental
control of the sympathetic and
parasympathetic divisions by the
ANS
Clinical Connections:
Acute Autonomic Paralysis
• Causes spinal shock with autonomic
effects of
– Paralysis of bowel and bladder
– Anhidrosis
– Loss of piloerection and sexual function
– Potentially severe hypotension
Clinical Connections:
Autonomic Dysreflexia (AD)
• Potentially life-threatening condition
associated with spinal cord lesions
above the sixth thoracic segment
• Characterized by high blood
pressure, severe headaches, goose
bumps, and sweating
Autonomic Dysreflexia
Clinical Connections:
Autonomic Dysreflexia (AD)
• Elicited by a noxious stimuli below level
of injury triggering sympathetic-driven
increase in blood pressure
• Disruption of the descending
parasympathetic fibers unable to
modulate
• Treated by immediately sitting person
with AD upright
Clinical Evaluation
of the Olfactory Nerve
• Test each nostril separately with a
familiar scent
• Olfaction, emotion, and memory
• Anosmia (inability to smell) may
occur with a common cold, trauma,
and some degenerative diseases
such as Parkinson's and Alzheimer's
Disorders of Eye Movement
• Opthalmoplegia – paralysis of one or
more of the extraocular muscles
• Strabismus – inability to direct both
eyes to the same object
– Lateral – due to paralysis of CN III
– Medial-due to paralysis of CN VI
• Diplopia – double vision
• Ptosis – weakness of levator
palpebrae superioris muscle
Clinical Evaluation of the
Trigeminal Nerve
• Corneal reflex
• Sensory tests for DCML and STT
modalities
• Palpate muscles of mastication, resist
jaw opening
Lesions of the Trigeminal Nerve:
Trigeminal Neuralgia (tic douloureux)
• No motor or sensory losses
• Excruciating bursts of pain, usually in
one of the three sensory distributions
of CN V
• Triggered by use of jaw, yawning,
hot and cold, light breeze on face
Lesions of the Trigeminal
Nerve:
Herpes Zoster Ophthalmicus
• Inflammatory and infectious disease
• 2–3 days of severe pain along
distribution of the opthalmic division
of CN V
• Rash follows in this distribution
• Can result in corneal damage
Clinical Evaluation of the Facial
Nerve
• Special sensory – taste
• Branchial motor – muscles of facial
expression
Lesions of the Facial Nerve:
Bell's Palsy
• Most common disease affecting facial
nerve
• Often caused by herpes simplex virus
• Acute onset
• Characterized by paralysis of facial
muscles, impaired corneal blink
reflex, and hyperacusis
Bell’s Palsy
Vestibulocochlear Nerve (VIII)
• Special sensory
• Conveys vestibular (equilibrium) and
cochlear (hearing/auditory)
information
• Nuclei located in caudal pons and
rostral medulla
• Clinical evaluation includes tests of
the ability to coordinate eye–head
movements and of hearing
Clinical Evaluation and Lesions
of the Glossopharyngeal Nerve
• Testing of gag reflex somewhat
unreliable as pharyngeal wall
innervated by CN IX and CN X
• Isolated lesions of CN IX are rare
Clinical Evaluation and Lesions
of the Vagus Nerve
• Observation of movements of the
soft palate
• Observation of vocal quality
• Lesions of CN X can produce
hoarseness of speech and difficulty
with swallowing
Palate drooped and deviated to
Unaffected side
Clinical Evaluation and Lesions
of the Accessory Nerve
• Muscle testing against resisted head
turning and shoulders shrugging
• Lesions can occur with surgical
procedures of the neck and with
trauma
Clinical Evaluation and Lesions
of the Hypoglossal Nerve
• Observation of tongue protrusion and
speech articulation
• Lesions result in atrophy of the
tongue and dysarthria – try saying
“late night downtown”
Tongue Protrusion
Clinical Connection:
Trigeminal Neuralgia
• Also called "tic douloureux"
• Disease of PNS affecting the
trigeminal ganglion or nerve
• Characterized by brief attacks of
excruciating pain in one or more
divisions of the trigeminal nerve
• Mechanisms and cause largely
unknown
Trigeminal Neuralgia
Clinical Connection:
Wallenberg's Syndrome
• Also called lateral medullary syndrome
• Typically caused by a vascular lesion,
occlusion of the posterior inferior
cerebellar artery
• Characterized by loss of pain and
thermal sense in ipsilateral face and
contralateral body due to damage of
ascending spinal trigeminal and STT
tracts
Wallenberg’s and Hypoglossal
Syndromes
Clinical Connection: Dysarthria
• Motor deficits in the production of
articulated speech
• Follows damage to UMNs or LMNs
subserving the muscles of articulation
• Could be caused by a variety of
pathologies including stroke, trauma,
disease processes
Clinical Connection:
Progressive Bulbar Palsy
• Motor system disease (combined UMN
and LMN signs) dominated by weakness
of the orofacial muscles
• Characterized by dysarthria, impaired
chewing and swallowing, atrophy and
fasciculations of tongue
• May present with pathological laughing
and crying
Clinical Connection:
Pseudobulbar Palsy
• Also called spastic bulbar paralysis
• Often caused by bilateral lesions of
internal capsule affecting
corticobulbar tracts
• Pathological laughing and crying
along with bilateral bulbar signs
Figure 15-17 Midbrain syndromes. (a) Occlusion of the
paramedian penetrating branches of the PCA results in superior
alternating hemiplegia (Weber's syndrome). (b) Occlusion of the
penetrating branches of the PCA that supply the tegmentum results
in Benedikt's syndrome.
Clinical Connection:
Weber's Syndrome
• Also called superior alternating
hemiplegia
• Often caused by infarction of
paramedian branches of the PCA
Clinical Connection:
Weber's Syndrome
• Structures damaged
– Descending tracts in cerebral peduncle,
nucleus for CN III
• Related symptoms
– Spastic hemiparesis of contralateral
body and lower half of face, ipsilateral
oculomotor palsy
Clinical Connection:
Benedikt's Syndrome
• Caused by occlusion of tegmental
branch of the PCA
• Structures damaged
– Nucleus for CN III, cerebellothalamic
tract
• Related symptoms
– Ipsilateral oculomotor palsy and
contralateral ataxia of the extremities
Medullary syndromes
Weber’s Syndrome