Clinical Connections.

Clinical Connections

Clinical Connection: Spina Bifida
Defective closure of the caudal neural tube Variabilility in severity Spina bifida oculta Spina bifida cystica Spina bifida with myelomeningocele Spina bifida with meningomyelocele Spina bifida 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 Maria = complete T6 transection (skiing accident) Loss of Bowel, bladder, genital fxn, walking, breathing problems Jon = tumor on SC = sensory loss

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 Chain from bike wound  tetanus Dented food can  Botulism

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 Proprioception and light touch there/spared Pain, temp and motor control in LE gone Spinal shock, recovers quickly sometimes, unpredictably

Clinical Connection: Herniation of the Vertebral Disc
Displacement of disc tissue from normal position between vertebral bodies Nuclear protrusion mild Disc prolapse more severe More mobile = more likely to herniate C5/6, 6/7, L5/S1

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 Usually NOT trauma/severing More of cytotoxic death

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 More likely in most mobile Thinning of disc, degeneration

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 More pressure => Bone outgrowth of veterbral body, narrows space => numbness, pain, weakness

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 From Extensive lesions of posterior thalamus (from stroke)  Hemi-anesthesia = profound to total loss of somatic sensation over CL head and body Sensory Ataxia = Motor incoordination, loss of propr. info Thalamic pain = excruciating, unrelenting pain on half of body Medications to modulate pain unsuccessful, pain location in highest portion

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 Resting tremor – more obvious spontaneous tremor at rest Attention tremor – more obvious when you intend to do a movement Nystagmus – jerky, rhythmic, jumping of eyes

Tremor-rhythmic, alternating movement of a body part
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) Turret’s – can suppress tics, but must let it out eventually, takes a lot of energy

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 Motor Aphasia = lack of speech (Brocha’s aphasia), comprehension isn’t affected

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

Figure (a) Area of the left cerebral hemisphere 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 lobe and the temporal lobe. Abbreviation: BA, Brodmann's area. (Adapted from Bowman, J. P., and Giddings, D. F. Strokes: An Illustrated Guide to Brain Structure, Blood Supply, and Clinical Signs. Prentice Hall, New Jersey, 2003.)

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 Tetraplegia = quadrplegia = paralysis of 4 limbs Strophy = no static, low level tone contraction = rapid and severe Disuse atrophy = longer to appear and not as obvious, not LMN

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 AIDP = rapidly progressing (starts in toes) = Never fully recover, neuropathic pain, weakness, numbness, autonomic problems (sweating in feet)

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 Dysphagia = problems with swallowing Dysphasia = problems with language (understanding or getting words out) Dysarthia = problems with speaking (muscles of speech weak/stiff, cannot produce words)

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
Uses Gower maneuver to get up from floor

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 Diagnosis : bulbar signs = strange tongue motions

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 Hyperreflexia Poke muscle, readiness/tone to contract Damage to UMN pathway, develops spasticity Hypertonia = slowly flex elbow smooth vs fast flex/ext of elbow might catch and have more resistance

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
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
Figure (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 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

Rarely encountered lesion involving only one-half of the spinal cord

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 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 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.

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

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 The cavity in syringomyelia often interrupts spinothalamic afferents crossing in the ventral white commissure.

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

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 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
Figure 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

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