Neurology Flashcards
Frontal lobe function
Planning and execution of movement
speech
smell
problem solving
Parietal lobe function
Sensory input - touch
pressure
Body orientation
Temporal lobe function
Understanding language
Behavior
Hearing
Memory
facial recognition
Occipital lobe function
Vision
Color perception
Cerebellum function
Balance
Coordination of voluntary movement
Fine muscle control
Brain stem function
Breathing
Temperature
Digestion
Alertness/sleep
Swallowing
Hippocampus function
Memory
Amygdala function
Emotions
Thalamus function
Relay signals from lower brain to cortex
Basal ganglia function
Sorting, evaluating and executing motor functions, filtering out unwanted movement
parts of basal ganglia
caudate nucleus
putamen
globus pallidus
subthalamic nucleus
substantia nigra.
grey matter content
neuronal cell bodies
white matter content
neuronal axons forming tracts
what does the sympathetic nervous system do to the eye?
Causes pupillary dilation - Mydriasis by the pupillary dilator muscle
Innervation of the pupillary dilator muscle
Postganglionic sympathetic fibers project from the superior cervical ganglion. Fiber travel with the ophthalmic artery, forming a number of long ciliary nerves that supply the dilator pupillae muscle
what does parasympathetic nervous system do to the eye
Cause pupillary constriction by sphincter pupillae muscle - Miosis
innervation of pupillary sphincter muscle
Receives parasympathetic innervation via the short ciliary nerves. Fibers originate from the Edinger-Westphal nucleus of cranial nerve III.
Pupillary accommodation
Contraction of ciliary muscle: near vision
Relaxation of ciliary muscle: fare vision
innervation og cilliary muscle
These parasympathetic fibers arise from cranial nerve V, also known as the nasociliary nerve of the trigeminal.
Areas of lesion causing effect on pupil
Hypothalamus controls - PSNS - constriction
Paravertebral SNS - dilation
Neck - fibers run with ICA
Trauma to orbit
name of pupillary constriction and dilation
dilation: Mydriasis
constriction: miosis
name of unequal size of pupils
Anisocoria
part of pupil is missing name
coloboma
describe the light pupil reflex
- light in right eye
- AP in pretectal nuclei
- signal from pretectal to EW nuclei - AP
- EW generate AP through the CN III
- Oculomotors nerve causes miosis
causes of mydriasis
CN 3 lesion
Adie’s pupil
Migraine
Drugs
seen in complete CN 3 lesion
mydriasis
ptosis
impaired eye movement
loss pupil reflex
drugs causing mydriases
Anticholinergics
TCA
NSAIDS
oral contraceptives
Antihistamins
causes of miosis
Horners syndrom
Argyll Robertson pupil
Drugs
content of facial nerve?
Motor fibers
Taste fibers - visceral afferent
Parasympathetic - visceral efferent
path of facial nerve motor nerve
from lateral brain
cerebellopontine angle
internal auditory meatus
facial canal
exit through stylomastoid foramen
path of parasympathetic fibers of facial nerve
With facial nerve into internal auditory meatus
what part og tongue is innervated by the facial nerve?
anterior 2/3
what is bells palsy
acute paralysis of the face related to a inflammation or swelling. usually unilateral.
etiology of bells palsy
viral infections: HSV VZV + others
what is bells phenomenon
attempt to close eyes and show teeth one eye can’t close and eyeball roles back
treat bells palsy
protect eye when sleeping + eyedrops
high dose prednisolone 10 days
antiviral therapy if known virus
Ramsay hunt syndrom
herpes zoster infection affecting the geniculate ganglion sudden severe pain, eruption of vesicle in external ear
deafness may be an outcome if CN VIII involvement
hemifacial spasm
- unilateral clonic spasms from orbicularis occuli then to rest of face
- contractions are irregular and increases with emotional stress and fatigue
- cause: vascular comprssion like tumor
vertigo dizziness
Room is spinning due to loss of orientation of body in space
causes of Central vertigo
■ Tumor (astrocytoma)
■ Cerebrovascular disorders
● Stroke
● Vertebrobasilar insufficiency
● TIA
■ Migrainous vertigo
■ Drugs/toxins
■ Multiple sclerosis (demyelination)
■ Inflammation (meningitis, cerebellar abscess)
■ Trauma
etiology of peripheral vertigo (85%)
■ Idiopathic
■ Menière’s
■ BPPV (benign paroxysmal positional vertigo)
■ Trauma
■ Drugs: streptomycin, quinine, salicylates
■ Labyrinthitis
■ Vestibular neuronitis
■ Cerebellopontine angle tumors
● Acoustic neuroma
● Meningioma
non-vertigo dizziness
Psychogenic (diagnosis of exclusion)
■ Depression
■ Anxiety etc
Vascular
■ Orthostatic hypotension
■ Arrhythmia
■ CHF
■ Aortic stenosis
■ Vagovagal episodes
Ocular
■ Decreased visual acuity
nystagmus in central vs peripheral nystagmus
central: Bidirectional horizontal or vertical
Peripheral: Unidirectional horizontal or rotatory
6 things you compare central vs peripheral
imbalance
nausea vomiting
auditory symp
neurological sympt
compensation
nystagmus
Ménière disease is a
Ménière disease is a disorder caused by build of fluid in the chambers in the inner ear. It causes symptoms such as vertigo, nausea, vomiting, loss of hearing, ringing in the ears, headache, loss of balance, and sweating.
to differentiate vertigo from dizziness
vertigo: WORLD IS SPINNING
dizziness: unsteady or lightheaded
Plegia vs paresis
plegi: complete loss
paresis: loss of power
Different pareses/plegias
Hemiplegia/hemiparesis: unilateral weakness of the limbs
Monoplegia/monoparesis: weakness of one limb,
Paraplegia/paraparesis: weakness of both lower limbs,
Diplegia/diparesis: weakness of both upper limbs,
Quadriplegia/tetraplegia or quadriparesis/tetraparesis: weakness of all four limbs,
Lesion of the corona radiata and the internal capsule causes
contralateral severe spastic hemiparesis with involvement of the lower part of the face and the tongue
Isolated lesion of the corticospinal tract in the cerebral peduncle and lesion of the pyramid in the medulla cause
flaccid weakness, however the joint lesion of all descending tracts leads to spastic hemiparesis.
Unilateral lesion of the base of the pons causes
contralateral hemiplegia/paresis, often sparing the face
Bilateral lesion of the base of the pons causes
quadriparesis/plegia.
Unilateral lesion of the cervical spinal cord at the level of C1-4 segments causes
ipsilateral spastic hemiparesis.
Bilateral lesion of the cervical spinal cord at the level of C1-4 segments causes
spastic quadriparesis
Lesion of the cervical spinal cord at the level of C5-Th1 segments causes
spastic weakness of the lower limbs and flaccid weakness of the upper limbs
Lesion of the thoracic spinal cord causes
spastic paraparesis
Lesion of the lumbosacral spinal cord causes
flaccid paraparesis.
Lesion of spinal motoneurons and anterior roots causes
flaccid weakness of segmental
distribution (in the corresponding myotomes)
Polyneuropathy typically causes
distal symmetrical flaccid weakness of the limbs, first on the lower limbs.
most important symptom of UMNL and LMNL
UMNL: BABINSKY - positive pyramidal sign
LMNL: visible fasciculation’s
lateral corticospinal tract is for
distal limbs and fine manipulation
anterior/ventral corticospinal tract is for
trunk and upper leg muscles (posture locomotor)
UPNL paralysis:
LMNL paralysis:
UPNL paralysis: spasmic
LMNL paralysis: flaccid
spasmicity vs rigidity
Spasticity: resistance in one direction. Velocity-dependent.
Rigidity: resistance in all directions. Not velocity-dependent
fasciculation vs fibrillations
○ Fasciculations: Visible twitching of motor unit of muscle due to spontaneous firing of
action potentials from damaged nerve
○ Fibrillations: Non-visible twitching of individual muscle fibers when nerve is even more
damaged - only seen on electromyogram
main cause of UMNL
stroke
demyelination
ALS
man cause of LMNL
polio
west nail virus
spinomuscular athropy
cauda eq. syndrom
DM neuropathy
botulism
ALS
what are the two fibers innervated in a muscle
Intrafusal Gamma fibers: reflex
Extrafusal alpha fibers contraction
where does the corticospinal tract deccusate
in the pyramids (brainstem)
what is the cerebrobulbar tract?
goes from cortext to pons/medulla and innervate CN
destination of corticobulbar tract
CN 5
CN 7
Nucleus ambiguous: CN 9, 10, 11
CN 12
why is there athropy in UMNL
loss of usage
loss of Ach release causing no AP or protein synthesis,
80% muscle loss
pathophysiology of fasciculations?
no Ach causes increase in R formation and increased mechanical sensitivity - tapping causes activation of reseptorc opening Na channels and AP
why is there spasmic paralysis in UMNL
because of less inhibitory signals from medullary reticulospinal tract causing hyperflexia and hypertonia
which side is the speech senter on?
LEFT hemisphere is dominant in most people
what is aphasia
Aphasia is a speech disorder with an inability to comprehend and/or formulate language. It is caused by
lesions of cortical speech centers and their connections
Broca’s and Werncks aphasia is?
Broca: Expressive
Wernicks: receptive
Areas in Brocas
BA 44
BA 45
areas in wernicks
WA 22
WA 39
WA 40
BA aphasia present?
know what do say but cant say it
NON FLUENT
skjønner men finner ikke ord
WA aphasia present?
difficulty understanding and finding right words, mix up words
snakker om helt rare ting
causes of aphasi
stroke
trauma
brain mass
neurodegenerativ disorders
encephalitis
conduction aphasia
understands and speaks but cant repeat
what supplies speech area?
middle cerebral artery
which artery infarct causes wernicks aphasia?
BRANCH OF MIDDLE CEREBRAL ARTERY: posterior temporal artery
etiology of conduction aphasia
Lesion of the arcuate fasciculus. Characterized by normal speech, but impaired repetition. Patient is aware and frustrated by this.
alexia without agraphia
Lesion in left occipital lobe usually due to infarct of the posterior cerebral artery.
The visual information cannot reach the language areas, and the patient is unable to read, but are able to
write (pure word blindness)
how can you find out which side language senter is on?
dominant hand: right hand - left area
left hand: mix of both 70% left 15% right 15% bilateral
what connect BA and WE
arcuate nucleus
The anatomical basis of arousal is the
Ascending reticular activating system (ARAS),
composed of the pontomesencephalic reticular formation, monoaminergic networks of the diencephalon and the intralaminar and medial nuclei of the thalamus
Disorder of arousal
● Somnolence - Mildest form. Awakens with
verbal stimuli, but is asleep without stimuli.
● Stupor - Patient may open eyes to painful stimuli, verbal is not enough. Slow and inappropriate reaction to stimuli.
● Coma - Cannot be awakened. Abnormal posture (decorticate or decerebrate).
i. Coma I - Preserved brainstem reflexes
ii. Coma II - Lost brainstem reflexes
disorders of awakefullness
Persistent vegetativ state
akinetic mutism
confusion
delirium
locked in syndrom
define persistant vegetativ state
Awake but not awareness of their surroundings.
Rostral brainstem remains intact → Thermoregulation (hypothalamus), sleep-wake cycle, endocrine system, cardiorespiratory and other visceral functions are intact
when is a vegetativ state permanent?
> 30 days
decorticated position
stiff with bent arms, clenched fists, and legs held out straight. Sign of severe damage in the brain
decerebrated position
all limbs are stiff en extended. Results from a rostral brain stem lesion and leads to extension of all four limbs and opisthotonos (spasm of the muscles causing backward arching of the head, neck, and spine, as in severe tetanus)
causes of vegetativ state
Extensive functional or structural impairment of
cerebral cortex
- global cerebral ischemia
- hypoglycemia
- renal/hepatic failure
- post-convulsive state
- Wernicke’s encephalopathy
- final stages of cortical dementias)
○ Extensive white matter damage
○ Bilateral damage to the thalamus
define akinetic mutism
- Awake, but mute and does not move.
causes of akinetic mutism
Caused by bilateral interruption of connections between the supplementary motor
area, cingular region and midline nuclei of the thalamus
are you paralised in akinetic mutism
NO, because of withdrawal reflex to pain, suckling reflex, and grasp reflex
etiology of akinetic mutism
○ Jet bleeding
○ Bilateral ischemia in the anterior cerebral artery
○ Subfalcial herniation
○ Occlusive hydrocephalus
○ Butterfly tumors growing across the corpus callosum
○ Tumors of third ventricle
define delirium
Cannot focus, change or fix attention.
Disoriented and incoherent thinking.
Evolves over 24h.
Inversion of sleep wake cycle. sweating, tachycardia unstable BP
what do you have to have to be counscious`
awareness
arousal
alertness
memory
function of ascending reticuloactivating system (ARAS)
reflexes
sensory information
respiration
HR/BP
sleep cycle
consciousness
posture
composition of ARAS system?
medial column
lateral column
medial column
composed of A LOT of nuclei
4 things to look for first in an unconscious patient
looks like sleeping?
spontaneous movement?
respons to voice/stimuli?
respiration stable?
how do you examine a uncounscious patient?
- observe
- stabile ABC
- GCS
- signs of external rauma
- eye position and reflexes
- limb position and reflexes
- deep tendom reflex
GCS values
< 3 high rate of death
< 8 coma –> intubate
15 is normal
deep tendon reflexes?
There are five primary deep tendon reflexes: biceps, brachioradialis, triceps, patellar, and ankle.
brain stem reflexes
Pupillary Light Reflex.
Corneal Reflex
Oculo-vestibular Reflex
Pain Stimulus.
Gag Reflex.
Cough Reflex.
findings in an unconscious patient and their cause?
1. Pupillary constriction (light reactions are preserved!)
2. Pupillary dilation (NO pupillary light reactions)
3. Fixed, moderately dilated pupils
4. Skew deviation (eyes diverge in vertical direction, one down, the other up)
5. Persistent upward deviation
6. Persistent downward deviation
- Bilateral → hypothalamus and diencephalon damage. Unilateral: Horner’s
- tectum lesions
- lesion below tectum
- caudal part of brainstem and meso-diencephalon damage
- global cerebral ischemia
- hepatic coma
what are the two vestibular reflexes
- move head side to side, pupils should move in opposite direction.
- cold/warm water stimulus COWS
what type of unconsciousness is normally related to metabolic origin?
persistent vegetativ state also called unresponsive awakefullness syndrom
metabolic causes of unconsciousness
● Deficiency of essential substrates (glucose, oxygen, vitamin B12)
● Exogenous toxins (eg. drugs, heavy metals, solvents)
● Endogenous toxins/systemic metabolic diseases (eg. uremia, hepatic encephalopathy, electrolyte
imbalances, thyroid storm
how can you diff between structural defect or coma due to hypoglycemia?
pupillary relex normally intact f hypoglycemia
what glucose level causes coma?
< 0.6 mmol/L
what is seen in hyperglycemia
hyperosmolar effect can cause coma. Can cause involuntary movements, seizures and hemiparesis
symptomes in ketoacidosis
Symptoms: dehydration (due to osmotic diuresis), fatigue, weakness, headache, abdominal pain,
Kussmal breathing, confusion, coma
