1 - Pathology Flashcards
What are the types of Cerebral Vascular Accidents (CVA)?
1) Strokes: bleeds and blocks -> bleeds from aneurysms or trauma, 80% fatal; blocks from thrombus(slow) or embolus(fast)
2) Cardiac Arrest: loss of consiousness temporary, focal deficit resolves temporary memory disturbance associated with hippocampus deficit
* * hemorrhage may appear quickly, but infarct won’t show for 6-8hrs; Mass Effect can cause brain displacement and 2nd injuries
What is a capsular infarct?
This is an infarct in an artery supplying the deep tissue of the brain (capsule). This area is supplied by penetrating branches of the ICA, middle cerebral, medial striate and lateral striate, and/or anterior choroidal arteries.
The neurologic deficit will be driven by the specific area affected.
What is Horner’s Syndrome?
-Horner’s Syndrome: disruption of sympathetic innervation of the face due to lesions along the path (downward pathways, T1-L3 cord, superior cervical sympathetic trunk)
-presents with PREMD
Pseudoptosis-> eyelid droops due to superior tarsal muscle
Redness-> flushing of face and conjunctiva via vasodilation
Enopthalmos-> sinking of eyeball into orbit due to smooth muscles
Miosis-> constriction
Dryness-> loss of sweat gland secretion
Describe the clinical presentation of a lesion to the unilateral, medial Medulla.
Ipsilateral Alternating Hemiplegia-> area of injury is supplied by Anterior Spinal Artery and affects the unilateral pyramid and CN XII paths
CN XII: damage results in IPSILATERAL weakness in the muscles of the tongue -> tongue deviation to SAME side
Pyramid: damage results in CONTRALATERAL weakness to skeletal muscles through interference with Corticospinal Tract (prior to decussation)
What is the clinical presentation of Wallenberg’s Syndrome?
Unilateral lesion to Lateral Medulla: results in damage to numerous sensory and motor nuclei; area is supplied by Anterior Spinal Artery and R/L Vertebral Artery
Spinal V Nuclei: loss of sensation to ipsilateral face
Spinothalamic tract: loss of pain, thermal, light touch to contralateral body
DA: Ipsilateral Horner’s Syndrome-> PRE MD
N. Ambiguus: ipsilateral muscle weakness to palate, pharynx and larynx muscles
ICP: ipsilateral ataxia and hypotonia
Vestibular nuclei: vertigo and nystagmus (abnormal eye mvmt)
What is the pathophysiology of a concussion?
- rapid acceleration/deceleration can cause rotation of the neuroaxis, particularly at the flexure of the brainstem and diencephalon
- this causes rapid opening of ion channels and release of glutamate
- these neurotransmitters then cause a rapid increase in metabolic rate, a subsequent decrease in O2 levels, which cause the symptoms of a concussion
- this increased metabolic rate can result in prolonged (days) decrease in cerebral glucose -> this may be true with NO overt symptoms
What are the clinical categories of consciousness?
1) Coma: unarousable state with no sleep/wake cycle and no means of communicating with environment
2) Vegetative State: state where the patient is unable to communicate with the environment in any way, but can open eyes (even in response to stimuli) and can have a normal sleep/wake cycle
3) Minimally Conscious State: variable and transient state where the patient can open their eyes, has a sleep/wake cycle, can feel pain and will go through periods of being able to communicate verbally or through motions, but these periods may be followed by relapses of a more unresponsive state
4) Locked-In Syndrome: patient is fully conscious and aware of their surroundings, but is unable to communicate except through eye movements
What are the typical presentations of LMN and UMN injury?
LMN: injury leads to cell death and LOWERING of activity -flaccid paralysis -hypotonia -reduced/absent myotatic reflex -fasciculations -rapid muscle atrophy UMN: loss of control of the pathway; so HIGH activity -spastic paralysis -hypertonia -hyperative myotatic reflexes -increased resistance to passive movement -Babinski sign, Clasp-knife syndrome, -late muscle atrophy
What is the clinical presentation of Sensory Ataxia? What are some causes?
- Ataxia: gross lack of coordination in voluntary movements (frequently involving deficits of cerebellar or vestibular function)
- Sensory Ataxia: damage to posterior column/medial meniscus causes 1) unsteady gait (broad based, stomping), 2) Romberg Sign (falls over when eyes shut)
- lesions to posterior column compromise conscious proprioception, so without sight, vestibular system cannot maintain posture
Describe the presentation of a spinal cord transection.
- Initial: spinal shock-> complete flaccid paralysis from level of transection and down; may be due to acute interruption of descending excitatory pathways
- weeks-months: UMN signs begin to show and dominate; babinksi is usually one of the first sign to develop, with spasticity and hyperreflexia developing over several months
Describe the presentation of Brown-Sequard Syndrome.
-spinal hemisection (penetrating wounds, compression, fracture, MS
-characterized by differing symptoms on either side of the body below the level of the lesion -> due to levels of crossing tracts
IPSILATERAL:
Posterior Column: loss of light touch, vibration, conscious prop
LCST: UMN signs: loss of motor control skeletal muscles
Anterior Horn: LMN signs: loss of skeletal muscle innervation/reflex AT LEVEL
CONSTRATERAL-
ALSTT: loss of pain, thermal and 2-pt touch
AT LEVEL-
Anterior White Commissure: loss of pain, thermal and 2-pt touch at level
Describe the presentation of Combined System Disease.
- subacute combined degeneration-> bilateral degeneration of Posterior Column and LCSTT due to B12 deficiency (myelin production)
- Sensory disturbance: loss of light touch, vibration in lower limbs; Romberg Sign (conscious proprioception); parasthesias (pins/needles) lower limbs; numbness and coldness in feet
- Motor disturbance: UMN signs, spastic paralysis, babinki, hyperactive reflexes, MAY convert to LMN signs due to peripheral neuropathy
What is the clinical presentation of Tabes Dorsalis?
- CNS/tertiary syphilis
- infection/destruction of DRG of lumbosacral region -> progresses to degeneration of Fasciculus Gracilis
- Sensory: loss of light touch, vibration, conscious proprioception for lower limb (Romberg sign); insensitivity to pain (?)
- Motor: LMN signs
What is the presentation of Syringomyelia?
- central gliosis and expansion of the central canal (fluid filled cavity->syrinx) due to unknown mechanism
- causes damage to Anterior White Commissure-> bilateral and symmetrical loss of pain and thermal sensation in the dermatomes associated with the affected cord segments
- Sensory Dissociation: tactile sense is preserved (posterior column)
- can progress to additional signs (LMN/UMN) as lesion expands
What is a wedge compression fracture.
- flexion fracture
- > 3mm compression of anterior body
- posterior column fine
- stable unless >25% compression
What is a flexion teardrop fracture.
- flexion fracture
- anterior, inferior corner of vertebra is broken off
- all ligaments in area are torn
- typical of lower c-spine from forceful flexion (diving into pool)
- bad injury: vertebral artery damage, cervical instability
What is a bilateral facet dislocation?
- extreme hyperflexion
- anterior dislocation of one vertebra over another
- Locked vs Perched Facets: locked means the spinous process is jammed into the anterior margin of the lower spinous process
- HIGH risk of cord injury
What is a Clay Shoveler’s fracture?
- flexion fracture
- fracture of spinous process from C6-T1
- powerful hyperflexion with paraspinous muscle contraction
- no neuro deficit; stable
What is a Unilateral Facet Dislocation?
- flexion fracture w/ rotation
- torn apophoseal ligament and anterior dislocation of the vertebral body <50% of width
- typically stable
What is a Hangman Fracture?
- extension fracture
- fracture at pedacle/pars interarticularis of C2 (axis)
- associated with hanging or MVA (chin hits dashboard)
- unstable, anterior longitudinal ligament avulses from vertebra
What is a Jefferson Fracture?
- compression fracture of C1
- fracture of anterior and posterior arches of C1, associated with tearing transverse ligament (cruciform)
- direct blow to top of head (diving)
- unstable is posterior longitudinal ligaments are torn
What is a Burst Fracture?
- compression fracture of C3-C7
- axial compression leading to fracture/dislocation
- cord injury related to posterior fragments
What are the different odontoid fractures?
Type 1: tip of odontoid (~)
Type 2: base of odontoid (unstable)
Type 3: into the body of the axis (best prognosis)
What are the clinical presentations for the different types of cerebral hemorrhage?
Epidural: rupture of MMA leads to fluid build up BETWEEN SUTURE line
- Clinical: period of lucidity, followed by unconscious state and potential for coma; Cushing Syn->hypertension w/ bradycardia; blown pupil of compression CN III
- Subdural: rupture of branching/cerebral veins as they cross from sinus to SAS; creates crescentic pool that CROSSES suture lines
- Clinical: slow onset (days-wks), presents w/ worsening headache, degenerating consciousness
- Subarachnoid: damage to arterial/venous vessels/anyeurism in SAS, creates large pool that fills cisterns and convexities
- Clinical: rapid onset (arterial), “worst headache of my life,” bloody CSF, communicating hydrocephalus
- Parenchymal: cerebral HPTN, diabetes, tumors or amyloid angiopathy weakens walls and creates microaneuryms; rupture to cause intracerebral hemorrhage
- Clinical: compression of brain mater causes symptoms; typically in deep structures (basal ganglia, putamen, thalamus, internal capsule)
