Miscellaneous Flashcards
Aphasia vs dysarthria
Aphasia is higher order inability to speak (language deficit)
Dysarthria is motor inability to speak (movement deficit)
Where are broca’s and wernicke’s?
In dominant hemisphere (if R handed, your dom hemisphere is L)
Motor speech is Broca - Frontal lobe above sylvian fissure
Associative auditory cortex is Wernicke - temporal below sylvian. Borders parietal too. Behind primary auditory cortex.
Broca’s aphasia
1) No fluency
2) Yes comprehension
3) No repetition
Inferior frontal gyrus
Broca is Broken Boca
Wernicke aphasia
1) Yes fluency
2) No comprehension
3) No repetition
Superior temporal gyrus
Wernicke is Wordy but makes not sense. Wernicke is What???
Conduction aphasia
1) Yes fluency
2) Yes comprehension
3) No repetition
Arcuate fasciculus
Can’t repeat phrases such as No ifs, ands, or buts
Global aphasia
1) No fluency
2) No comprehension
3) No repetition
AF, Brocas and Wernicke affected
Transcortical motor aphasia
1) No fluency
2) Yes comprehension
3) Yes repetition
Transcortical sensory aphasia
1) Yes fluency
2) No comprehension
3) Yes repetition
Mixed transcortical aphasia
1) No fluency
2) No comprehension
3) Yes repetition
Broca and Wernicke involved. AF spared.
Kluver-Bucy Syndrome
Bilateral amygdala lesion
disinhibited behavior (hyperphagia, hypersexuality, hyperorality)
Associated with HSV1
Frontal lobe lesion
Disinhibition and deficits in concentration, orientation, judgment. May have reemergence of primitive reflexes
Nondominant parietal-temporal cortex lesion
Hemispatial neglect syndrome (agnosia of contralateral side of the world)
lesion to dominant parietal-temporal cortex
Agraphia, acalculia, finger agnosia, L-R disorientation
Gerstmann Syndrome
Lesion to reticular activation system (midbrain)
Reduced levels of arousal and wakefulness (coma)
Mammilary body lesion bilateral
WKS - confusion, ophthalmoplegia, ataxia; memory loss (anterograde and retrograde amnesia), confabulation, personality changes
Associated with thiamine deficiency and excessive EtOH use. Can be precipitated by giving glucose without B1 to a B1 deficient patient
CAN of beer - Confusion, Ataxia, Nystagmus
Basal ganglia lesion
May cause tremor at rest, chorea, athetosis
PD, HD
Cerebellar hemisphere lesion
Intention tremor, limb ataxia, loss of balance; damage to cerebellum leading to ipsilateral deficits. Fall toward side of lesion
Cerebellar hemispheres are laterally located - affect lateral limbs
Cerebellar vermis lesion
Trunctal ataxia, dysarthria
Vermis is centrally located - affected central body
STN lesion
Contralateral hemiballismus
Hippocampus lesion bilateral
Anterograde amnesia - inability to make new memories
Paramedian pontine reticular formation lesion
Eyes look away from side of lesion
Frontal eye field lesion
Eyes look towards lesion
MCA stroke
1) Motor cortex - upper limb and face: Contralateral paralysis of upper limb and face
2) Sensory cortex - upper limb and face: Contralateral loss of sensation of upper limb and face
3) Temporal lobe (Wernicke), Frontal lobe (Broca): Aphasia if in dominant (usually left) hemisphere. Hemineglect if lesion affects nondominant (usually Right) hemisphere
ACA stroke
1) Motor cortex - lower limb: Contralateral paralysis of lower limb
2) Sensory cortex - lower limb: Contralateral loss of sensation of lower limb
Lenticulo-striate artery stroke
Striatum, internal capsule: Contralateral hemiparesis/hemiplegia
Common location of lacunar infarcts secondary to unmanaged HTN
Anterior Spinal Artery stroke
1) Lateral corticospinal tract - Contralateral hemiapresis of upper and lower limbs
2) Medial lemniscus - reduced contralateral proprioception
3) Caudal medulla, hypoglossal nerve - ipsilateral hypoglossal dysfunction (tongue deviates ipsilaterally)
Stroke is commonly bilateral
Medial Medullary Syndrome - Caused by infarct of paramedian branches of ASA and vertebral arteries
PICA stroke
Lateral medulla - vestibular nuclei, lateral spinothalamic tract, spinal trigeminal nucleus, nucleus ambiguus, sympathetic fibers, inferior cerebellar peduncle
Vomiting, vertigo, nystagmus; reduced pain and temp senseation from ipsilateral face and contralateral body; DYSPHAGIA, HOARSENESS, lower gag reflex; ipsilateral Horner; ataxia, dysmetria
Lateral Medullary (Wallenburg) Syndrome - Nucleus Ambiguus effects are specific to PICA. Don’t PICK A (PICA) HORSE (horseness) that CANT EAT (dysphagia)
AICA stroke
1) Lateral pons - cranial nerve nuclei; vestibular nuclei, facial nucleus, spinal trigeminal nucleus, cochlear nuclei, sympathetic fibers
Vomiting, vertigo, nystagmus. PARALYSIS OF FACE. reduced lacrimation, salivation. Reduced taste from anterior two thirds of tongue
Ipsilateral reduced pain and temp of the face, contralateral loss of pain and temp of body
2) Middle and inferior cerebellar peduncles - ataxia, dysmetria
Lateral Pontine Syndrome - facial nucleus effects are specific to AICA lesions. Facial droop means AICA’s pooped.
PCA stroke
Occipital cortex, visual cortex - Contralateral hemianopia with macular sparing
Basilar stroke
Pons, medulla, lower midbrain, corticospinal and corticobulbar tracts, ocular cranial nerve nuclei, PPRF
Preserved consciousness and blinking, quadriplegia, loss of voluntary facial, mouth, and tongue movements
“locked in”
ACom lesion
Most common lesion is aneurysm. Can lead to stroke. Saccular (berry) aneurysm can impinge cranial nerves
Visual field defects
Lesions are typically aneurysms not strokes
PCom lesion
Common site of saccular aneurysm
CN3 palsy - eye is down and out with ptosis and mydriasis
Lesions are typically aneurysms not strokes
Where does most CSF drain?
Superior sagittal sinus via arachnoid granulations
CSF route
Lateral ventricle to 3rd ventricle via R and L interventricular foramina of Monro
3rd to 4th via cerebral aqueduct of Sylvius
4th to subarachnoid space via Foramina of Luschka (lateral) and Magendie (medial)
Communicating hydrocephalus
Lower CSF absorption by arachnoid granulations leads to higher ICP, papilledema, herniation (think arachnoid scar post meningitis)
NPH
Type of communicating hydrocephalus
Affects the elderly; idiopathic; CSF pressure elevated only episodically; does not result in increased subarachnoid space volume.
Expansion of ventricles distorts the fibers of the corona radiata (nerve fibers running along ventricles) leading to triad of urinary incontinence, ataxia and cognitive dysfunction (sometimes reversible)
LP improves symptoms
Tx = VP Shunt (shunt CSF from ventricles into peritoneum)
Noncommunicating (obstructive) hydrocephalus
Caused by structural blockage of CSF circulation within ventricular system (stenosis of aqueduct of Sylvius; colloid cyst blocking foramen of Monro)
Ex vacuo ventriculomegaly
Appearance of increased CSF on imaging, is actually due to decreased brain tissue (neuronal atrophy)
Ex = AD, advanced HIV, Pick Disease
ICP normal. Triad not seen.
ALS lesion pattern
Coritcospinal (UMN signs) and ant motor horn (LMN signs)
No sensory (distinguishes from syringomyelia) or oculomotor deficits. Can be caused by defect in superoxide dismutase I.
Fasciculations with eventual atrophy and weakness of hands; fatal
Riluzole modestly increases survival by lowering presynaptic glutamate release (it’s a glut antag)
Complete occlusion of ASA
Spares dorsal column and Lissauer tract; upper thoracic ASA territory is watershed area as artery of Adamkiewicz supplies ASA below T8
Tabes Dorsalis
Caused by tertiary syphilis. From degeneration (demyelination) of dorsal columns and roots leading to impaired sensation and proprioception, progressive sensory ataxia (inability to sense or feel the legs leading to poor coordination)
Associated with Charcot joints, shooting pain, Argyll pupils
Exam shows no DTRs and positive Romberg
Syringomyelia
Syrinx expands and damages anterior white commissure of spinothalamic tract (second order neurons) leading to bilateral loss of pain and temperature sensation (C8-T1)
Seen with Chiari I malformation
Can expand and affect other tracts
Brown Sequard
Hemisection of spinal cord
1) Ipsilateral UMN signs below level of lesion (due to corticospinal tract damage)
2) Ipsilateral loss of tactile, vibration, proprioception sense below level of lesion (dorsal column damage)
3) Contralateral pain and temp loss below level of lesion (spinothalamic lesion)
4) Ipsilateral loss of all sensation at level of lesion
5) Ipsilateral LMN signs (flaccid paralysis) at level of lesion
If lesion is above T1 you might see Horner due to damage of oculosympathetic pathway
Friedreich Ataxia
Auto recessive GAA repeat disorder on chromosome 9 in gene that encodes frataxin (iron binding protein)
Leads to impairment in mitochondrial functioning. Degeneration of multiple spinal cord tracts leads to muscle weakness and loss of DTRs, vibratory sense, proprioception
Staggering gait, frequent falling, nystagmus, dysarthria, pes cavus, hammer toes, diabetes mellitus, hypertrophic cardiomyopathy (cause of death). Present in childhood with kyphoscoliosis
If you cant regulate Fe right you get more ROS due to Fentin reaction
Friedrich is Fratastic (frataxin); he’s your favorite frat brother, always staggering and falling but he as a sweet, big heart.
Dermatome landmarks
C2 - posterior half of a skull cap
C3 - high turtleneck shirt
C4 - low collar shirt
T4 - at nipple
T7 - xyphoid
T10 - umbilicus
L1 - inguinal ligament
L4 - includes kneecaps
S2,3,4 - erection and sensation of penile and anal zones
Clinical reflexes
Biceps - C5 nerve root
Triceps - C7 nerve root
Patella - L4 nerve root
Achilles - S1 nerve root
S1,2 - buckle my shoe (Achilles)
L3,4 - kick the door (patellar)
C5,6 - pick up sticks (biceps)
C7,8 - lay them straight (triceps)
L1,L2 testicles move (cremaster)
S3,S4 winks galore (anal wink)
Cranial nerve nuclei locations
Midbrain - 3,4
Pons - 5,6,7,8
Medulla - 9,10,12
Spinal cord - 11
Lateral nuclei are sensory (alar plate). Medial are motor (basal plate)
CN 1 exit
Cribiform plate
CN 2-6 exit
Middle cranial fossa through sphenoid bone
Optic canal = 2
Superior orbital fissure = 3, 4, V1, 6
Foramen Rotundum = V2
Foramen Ovale = V3
Foramen spinosum = middle meningeal artery
CN 7-12 exit
Posterior cranial fossa through temporal or occipital bone
Internal auditory meatus = 7, 8
Jugular foramen = 9, 10, 11, jugular vein
Hypoglossal canal = 12
Foramen magnum = spinal roots of 11, brain stem, vertebral arteries
Vagal nuclei
1) Nucleus Solitarius - Visceral sensory information (taste, baroreceptors, gut distention) 7, 9, 10
2) Nucleus ambiguus - Motor innervation of pharynx, larynx, upper esophagus (swallowing, palate elevation) 9, 10, 11 (cranial portion)
3) Dorsal motor nucleus - sends autonomic (parasympathetic) fibers to heart, lungs, upper GI - 10 only
CN V lesion
Jaw deviates toward side of lesion due to unopposed force from the opposite pterygoid muscle
CN X lesion
Uvula deviates away from side of lesion. Weak side collapses and uvula pulls away
CN XI lesion
Weakness turning head to contralateral side of lesion (SCM). Shoulder drop on side of lesion (trap).
Left SCM contracts to help turn the head to the right.
CN XII lesion (LMN)
Tongue deviates toward side of lesion (“lick your wounds”) due to weakened tongue muscles on affected side
Cavernous Sinus Syndrome
Presents with variable ophthalmoplegia, lower corneal sensation, Horner and occasional decreased maxillary sensation. Secondary to pit tumor mass effect, carotid-cavernous fistula, or cavernous sinus thrombosis related to infection.
CN 6 is most susceptible to injury
Cavernous sinus
Collection of venous sinuses on either side of pit. Blood from eye and superficial cortex leads to cavernous sinus then IJ vein
CN 3, 4, V1, 6 and sometimes V2 plus postganglionic sympathetic pupillary fibers enroute to orbit all pass through it
Cavernous portion of internal carotid is here too.
Hearing loss types
1) Conductive - Rinne is abnormal ( bone is more than air). Weber localizes to affected ear
2) Sensorineural - Normal rinne (air is more than bone). Weber localizes to unaffected ear.