Test 2 Clinicals Flashcards
Neural Tube Defects
1) Failure of neural tube to close
Rachischisis
1) Neural tube defect
- neural folds don’t join at midline
- undifferentiated neuroectoderm remains exposed
2) Rachischisis totalis
- AKA holorachischisis
- extreme form
- entire spinal cord remains open
3) Rachischisis partialis
- AKA merorachischisis
- spinal cord is partially open
Anencephaly
1) Neural tube defect
- anterior neuropore doesn’t close
- skull and brain do not develop
2) Anencephaly (Without brain)
- meroanencephaly (without part of brain)=more accurate
- brainstem intact but missing forebrain and cerebellum
Rachischisis vs Meroanencephaly
1) Most cases, especially meroencephaly
- DEATH
Spina Bifida
1) Neural tube develops normal
BUT surrounding vertebrae not formed properly
2) Spina Bifida OCCULTA
-partially missing vertebral arches
-area of defect indicated by patch of dark hairs
3) Spina Bifida CYSTICA- enlargements that contain:
-only meninges and CSF (meningocele)
-Meninges, CSF, portions of spinal cord (MENINGOMYELOCELE)
How is sensory info brought to the spinal cord?
1) Cell bodies- posterior root ganglia
2) Central Processess
- through spinal cord
3) Peripheral Processes
- through spinal nerves to innervate body structures
Sensory input originates from?
1) Body surface (GSA)
2) Deep structures such as: (GSA)
- muscles
- tendons
- joints
3) Internal Organs (GVA)
Injury to peripheral nerves
1) motor or sensory deficits distal to lesion
2) most notable in extermaties seen as:
- motor deficits (flaccid paralysis)
- decrease or loss of spinal reflexes (hyperreflexia, hyporeflexia, areflexia)
- Anesthesia (loss of sensation)
- Paresthesia (abnormal sensations)
Lumbar puncture
1) Obtain CSF
2) AKA spinal tap
3) L3/4 or L4/5
Spinal Reflex composed of:
1) Sensory neuron
2) motor neuron
3) resultant muscle contraction
Artery of Adamkiewicz
1) large spinal medullary artery
2) seen at L2 on Left side
3) important source of blood supply to the cord
4) must be preserved during surgery
Central Cervical Cord Syndrome
1) Trauma:
-hyperextension of c-spine
-mechanical injury to cord
2) Causes
-occlusion or spasm of anterior spinal artery
3) results:
Bilateral damage to cervical cord
4) Symptoms:
-bilateral weakness of extremities (primarily arms, forearms, hands)
-patchy loss of sensation below lesion
-urinary retention
Spinal Nerves
1) Formed by meeting of anterior and posterior roots
2) each nerve contains:
- afferent fibers->sensory input from periphery
- efferent fibers-spinal motor neurons
3) Fibers + circuit in gray matter=basis for spinal reflexes
- tested in neurological exams
Deafferentation pain
1) Anatomic pathways for pain perception are Partially or completely disrupted:
- nerve rootlets, tracts and nerves
2) May develop after:
- amputation
- peripheral nerve injury
- lesion of central tracts resulting in hemi/para/quadraplegia
- damage to posterior roots
3) Perceived As:
- dull and aching
- pins and needles (sharp pain)
- searing
- burning sensations
4) mechanism for pain is due to combo of:
- increased sensitivity of the central neurons (central sensitization)
- plasticity changes in damaged cell groups
- decrease in descending inhibitors
- increase in facilitate at he lesion site
Motorcycle Accident
1) Forcefull separation (avulsion) of posterior roots from spinal cord
- most often in brachial plexus
2) Tx: DREZ procedure (AKA PREZ)
- dorsal root entry zone
- small electron placed in posterior horn at entry zone
- radiofrequency lesions made at level of separation
3) Significant or total relief from pain seen in 80-90%
4) Complications:deficits related to adjacent
- corticospinal tract
- cuneate fasciculus
5) Symptoms:
- Ipsilateral weakness of upper or lower extremity
- Ipsilateral UE conscious proprioception and vibratory sense (pts describe buzzing sensation)
Myasthenia gravis
1) Moderate to profound muscle weakness
- muscle fatigue, worse as day progresses
2) presence of circulating antibodies against nicotine receptors on postsynaptic membrane
3) Result
- blockage at neuromuscular junction
4) Most common
- 20-40 y.o
- younger patients may exhibit symptoms
3 characteristics of Myasthenia gravis
1) Muscle weakness
- wax and wane for periods of mins to several days
2 Muscles controlling eye movement involved first (40%) –>result in DIPLOPIA AND PTOSIS (85% of pts)
- muscles of pharynx or larynx, face, and extremities may eventually be involved
- always with ocular muscles
- exhibit dysarthria and dysphagia
3) Weakness to administration of drugs that ENHANCE cholinergic transmission
Spinal reflex
1) Afferent fibers in spinal nerves may:
- synapse on tract cells and relay info to higher levels of neuroaxis
-terminate on motor neurons or interneurons
BOTH participate in reflex circuit
2) Require:
- afferent fiber
- interneurons or motor neurons
- target tissue (skeletal muscle)
3) Intrasegmental:
- simple reflex confined to single cord level
4) Intersegmental
- complex reflex in multiple cord segments
5) Numerous reflex apart of standard neurologic exam
Muscle Stretch Reflex
1) AKA tendon reflex or deep tendon reflex
2) Stimulus
- stretch of a muscle spindle located within the muscle
- tapping any large tendon
- ex: Knee jerk or quad stretch reflex
3) Reciprocal inhibitions
- one group of muscles is excited
- other antagonist group inhibited
4) Autogenic Inhibition
- AKA inverse myotatic reflex
- Golgi tendon organ=receptor
- responds to high tension
Flexor reflex
1) AKA withdrawal reflex
- nociceptive reflex
2) stimulis
-cutaneous input
-response to nociceptive stimuli
-protects a body part by removing from source of injury
(TAC on ground)
Cross Extension reflex
1) Builds on flexor reflex
- involves muscle of the contralateral side of body
Radiculopathy
1) Damage to (one or more) nerve root
2) Common cause
- spondylosis
- intervertebral disk disease
3) Due to dermatomes:
- k/o single root-> not significant sensory loss
4) Main symptom= perception of pain
- sharp burning pain (“shooting pains”
5) Cervical pain found in
- base of neck,
- over should
- down the UE
6) Lumbar problems:
- low back pain
- pain radiating down the LE (SCIATICA)
Mononeuropathy
1) deficit reflecting one peripheral nerve
2) Caused by:
- trauma (most common)
- entrapment
- compression syndromes (carpal tunnel syndrome)
Deficits/symptoms:
A) deviation of tongue on protrusion (hypoglossal nerve)
B)loss of flexion
-adduction and extension of fingers (ulnar nerve)
- toes(tibial nerve)
C)loss of pronation of forearm and movement of fingers
D) loss of dorsiflexion of foot/toes
Carpal Tunnel Syndrome
1) Most common entrapment mono neuropathies
2) median nerve compressed->large sensory deficits
3) Symptom:
- numbness
- tingling
- pain from the thumb, index finger, middle finger
4) Tx:
- section transverse carpal ligament to relieve pressure on median nerve
Polyneuropathy
1) motor and sensory deficits
- reflect damage to multiple peripheral nerves
2) Most common cause:
- diabetes MELLITUS ->Distal Axonopathy-> distal portions of fibers affected first
- start in LE and progress to UE
- small diameter myelinated/unmyelinated fiber affected first
3) Symptoms: STOCKING-GLOVE SENSORY LOSS
- numbness and loss of pain and temp in feet up to knees
- same deficits in hands to forearm
- as disease progresses: large diameter fibers involved and vibratory and position sense diminished or lost.
Sensory Neuronopathy vs motor neuronopathy
BOTH-result in loss of function related to peripheral nerves
Sensory Neuropathy
- loss of cell bodies in DRG
- results in sensory loss in BOTH distal and proximal portions of an extremity
- can include all sensory modalities
Motor NEuronopathy
- loss of anterior horn motor nears
- restuls in: flaccid weakness, muscle fasciculations, evental muscle atrophy
Posterior Columns
1) Gracilis and Cuneate Fasciculus
2) composed of heavily myelinated Primary Sensory fibers
3) Convey
- proprioceptive
- tactile
- vibratory sense
Gracilis Fasciculus
1) part of posterior columns
2) T6 and below`
Cuneate Fasciculus
1) part of posterior columns
2) T6 and up
ALS
- composed of
- damage
1) Anterolateral system
- Lateral Spinothalamic Tract (Pain and Temp)
- Anterior Spinothalamic Tract (General Tactile)
2) Damage to ALS
- begins 2 segments below lesion
Syringomyelia
1) Cavitation/Crater of central regions of cord
- usually cervical region
2) TYPES:
NONCOMMUNICATING syringomyelia -no lining of ependyma cells thus NOT AN ENLARGEMNT OF CENTRAL CANAL VS Communicating Syringomeylia -cyst connects with central canal VS Hydrosyringomyelia -cavitation of central canal
3) Small syringomyelia
-damage fibers crossing AWC
==>BILATERAL DEFICIT
4) Large Syrinx
- AWC and extends into anterior horn
- results bilateral loss of sensory and weakness of corresponding extremities
- one anterior horn=ispsilateraL weakness of uE
- both ant. horns=bilateral weakness
5) Ex: Lesion in mid to low cervical areas
- pain and temp sensory-Bilateral
- shoulders and arms=CAPE DISTRIBUTION
Brown-sequard Syndrome
1) Functional Hemisection of spinal cord results:
- damage to lateral corticospinal tract, ALS, posterior columns
- Functional–>-cord is not perfectly cut always across but m injured/deformed by pieces of damaged vertebrae
2) Lesion on R C4-C5
- Hemiparesis or hemiplegia–>muscle weakness or paralysis
- loss of pain and temp on Left side (ALS damage)
- Loss of proprioception, vibratory sense and fine touch (Gracile and Cuneate fascicle damage)
3) NET RESULTS
- loss of functional on half of the spinal cord
High Cervical Cord Lesion
1) Catastrophic event-> can’t breath
2) Potential for total loss of:
- sensation for the body below the lesion
- voluntary motor control below the lesion
3) Phrenic Nucleus
- Central regions of anterior horn C3-37
- innervates diaphragm
- lesion=disconnects from centers of medulla that control breathing
Acute Central Cervical Spinal Cord Syndrome
1) AKA central Cord syndrome
- incomplete spinal cord injury
2) Caused by:
- hyperextension of neck that occludes blood supply to cord from anterior spinal artery
3) deficit reflects the region served by artery:
- Bilateral weakness of extremities (Upper more than lower)
- varying degree of pain and temp loss
- Bladder dysfunction
4) Most patients Recover most or all function within 4 to 6 days:
- LE return first
- Bladder function
- UE function LAST
- Pain and temp return at any time
- posterior column sensations not affected
Opoids vs Opiates
OPOIDS 1) Produced by body: (endogenous) 2) 5 receptors: -u (mu) -d (delta) K (Kappa) -sigma -Epsilon 3) exs: B-endorphin= u and D receptors Enkephalin= u and D receptors Dynorphin= K receptors
OPIATES
1) bind to opoid receptors from outside body
2) Stops pain/EFFECTIVE analgesic
3) derived from opium poppy
4) ex:
- heroin
- morphine
Intrathecal Injection
1) Spinal block during pregnancy (local)
- picks target
- potent analgesic effect
CIPA
1) congenital insensitivity to pain w/anhydrosis
- anhydrosis (can’t sweat=sympathetic function)
2) RARE Genetic defect
- autosomal recessive
3) Child can’t feel pain
- cant diagnose until later in life
- won’t cry to pain
- die secondarily (not directly from disease)
4) Abnormal development of nociceptive receptors and some sympathetic neurons
Endorphin
1) Opioid:
- Endogenous version of morphine (opiate)
Fibromyalgia
1) thought to be CNS issue
- idiopathic-don’t know what causes
2) Symptoms-Wide and varied; bilateral presentation
- musculoskeletal pain
- tired
- cognitive difficulty
- maybe genetic
- maybe triggered by infection
Allodynia thalami
1)hypersensitive to pain
pain resulting from stimulus that doesn’t always cause pain
-CNS processing pain in abnormal way
-causes free nerve endings to be more active
2) AKA hyperalgesia
3) ex: overresponsive to bruise
TENS
Transcutaneous Electrical Nerve Stimulation
- though to stimulate tactile afferent in pain gating
- reduces pain
- ex: rubbing injured area`
Thalamic pain syndrome
1) AKA dejerine roussy syndrome
2) Pain being stimulated from CNS (central pain)
- location of pain depends on where thalamus is damaged
3) Can result from Thalamic stroke
4) can’t be controlled
- meds help but limited
UMN lesion vs LMN lesion
1) UMN Symptoms: -Paralysis, spastic (muscle spasm) -Hyperreflexia (deep tendon reflex) -no muscle atrophy (except by disuse) -Abnormal reflex--> + Babinski Sign
2) LMN Symptoms: -Paralysis, flaccid -hyporeflexia -muscle atrophy -fasciculations (quiver)
Central Herniation
1) AKA transtentorial herniation
- supratentorial compartment
2) Elevated Intracranial pressure
- forces diencephalon down through tectorial notch
3) Symptoms:
- initially change in respiration
- eye movement irregular
- dilated pupils
4) As damage progresses downward:
- Cheyne-stokes respiration w/intermittent tachypnea and apnea
- loss of motor and sensory
- loss of consciousness
5) Immediate muses to decrease ICP
Uncal Herniation
1) uncut down over edge of tentorium cerebeli
2) most common cause:
-expanding hemorrhagic lesion in the hemisphere
3) Initially compresses midbrain
-not checked damage can extend into lower brainstem levels
4) Progresses:
-respiration affected
-abnormal reflexes
-rapid decline
4) Early signs:
-dilated pupil
-abnormal eye movement (oculomotor nerve), w/double vision ipsilateral to herniations
Followed by:
-weakness of Extremities opposites to dilated pupil
Upward Cerebellar Herniation
1) Mass in posterior cranial fossa
-force portions of cerebellum up through tentorial notch
-compress midbrain
2) Result:
-occlusion of branches of superior cerebellar artery w/ infraction of cerebellar structures
and/OR
-increase in ICP (vomiting, headache, lethargy, decreased level ofc consciousness)
Dejerine Syndrome
1) AKA medial medullary syndrome
-occluded anterior spinal artery
-bilateral deficits
2)Anterior Spinal Arteries service
Medial structures of medulla @ all levels
-pyramid
-medial lemniscus
-hypoglossal nucleus/roots
3) Symptoms:
-Contra hemiparesis (pyramidal and corticospinal damage)
-Contra loss of conscious prop and vibratory sense (ML)
-Deviation of tongue to psi side when protruded (hypoglossal root or nucleus injury)
Wallenberg Syndrome
1) AKA Lateral medullary syndrome PICA syndrome 2)Affect Posterolateral medulla -Rostral to obex -served by branches of PICA 3)) PICA serves -ALS -Spinal trigeminal Tract and nucleus -vestibular nuclei -Solitary tract and nucleus -Nucleus Ambiguus 4) Deficits: -contra loss of pain/temp of body (ALS) -Ipsi loss of pain/temp of face (Spinal Trigeminal Tract and nucleus) -some vertigo and nystagmus (vestibular nuclei) -loss of taste from ispilateral half of tongue (solitary tract/nucleus -Hoarsenss and dysphagia (nucleus ambiguous 5) Associated with Horner's syndrome
referred pain
1) Noxious stimuli that originates in visceral structure (heart/stomach)
- perceived by patients from somatic portion of body wall (skin, bones or skeletal muscles)
2) Pain in chest
- perceived as intense pressure that radiates down left arm
- indicates serious heart problem
Agina
1) Referred pain w/diseases of heart
2) Agina pectoris
- perceived as a pain of chest
- sternum and pectoral muscles
3) 80% of patients perceive agina as:
- squeezing sensation ordination from behind sternum
4) Also perceived:
- pain radiating down L arm
- Bilateral down both arms, neck, jaw, and temporomandibuular joints (RARE)
Baroreceptor Reflex
1) Hypertension
- abnormally elevated BP
- major health issue
- variety of causes
2) Hypotension
- abnormally low BP
