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
