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Neurology Flashcards

1
Q

Frontal lobe function

A

Planning and execution of movement
speech
smell
problem solving

PPSS

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2
Q

Parietal lobe function

A

Sensory input - touch
pressure
Body orientation

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3
Q

Temporal lobe function

A

Understanding language
Behavior
Hearing
Memory

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4
Q

Occipital lobe function

A

Vision
Color perception

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5
Q

Cerebellum function

A

Balance
Coordination of voluntary movement
Fine muscle control

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6
Q

Brain stem function

A

Breathing
Temperature
Digestion
Alertness/sleep
Swallowing

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7
Q

Hippocampus function

A

Memory

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8
Q

Amygdala function

A

Emotions

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9
Q

Thalamus function

A

Relay signals from lower brain to cortex

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10
Q

Basal ganglia function

A

Sorting, evaluating and executing motor functions, filtering out unwanted movement

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11
Q

parts of basal ganglia

A

caudate nucleus
putamen
globus pallidus
subthalamic nucleus
substantia nigra.

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12
Q

grey matter content

A

neuronal cell bodies

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13
Q

white matter content

A

neuronal axons forming tracts

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14
Q

what does the sympathetic nervous system do to the eye?

A

Causes pupillary dilation - Mydriasis by the pupillary dilator muscle

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15
Q

Innervation of the pupillary dilator muscle

A

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

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16
Q

what does parasympathetic nervous system do to the eye

A

Cause pupillary constriction by sphincter pupillae muscle - Miosis

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17
Q

innervation of pupillary sphincter muscle

A

Receives parasympathetic innervation via the short ciliary nerves.
Fibers originate from the Edinger-Westphal nucleus of occulumotor cranial nerve III.

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18
Q

Pupillary accommodation

A

Contraction of ciliary muscle: close/near vision

Relaxation of ciliary muscle: far vision

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19
Q

innervation of cilliary muscle

A

These parasympathetic fibers arise from cranial nerve V, also known as the nasociliary nerve of the trigeminal.

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20
Q

Areas of lesion causing effect on pupil

A

Hypothalamus controls - PSNS - constriction
Paravertebral SNS - dilation
Neck - fibers run with ICA
Trauma to orbit

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21
Q

name of pupillary constriction and dilation

A

dilation: Mydriasis
constriction: miosis

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22
Q

name of unequal size of pupils

A

Anisocoria

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23
Q

part of pupil is missing name

A

coloboma

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24
Q

describe the light pupil reflex

A
  1. light in right eye
  2. AP in pretectal nuclei
  3. signal from pretectal to EW nuclei - AP
  4. EW generate AP through the CN III
  5. Oculomotors nerve causes miosis
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25
Q

causes of mydriasis

A

Adie’s pupil
CN 3 lesion
Drugs
Migraine

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26
Q

seen in complete CN 3 lesion

A

mydriasis
ptosis
impaired eye movement
loss pupil reflex

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27
Q

drugs causing mydriases

A

Anticholinergics
Antihistamins
oral contraceptives
TCA
NSAIDS

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28
Q

causes of miosis

A

Horners syndrom
Argyll Robertson pupil
Drugs

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29
Q

content of facial nerve?

A

Motor fibers
Taste fibers - visceral afferent
Parasympathetic - visceral efferent

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30
Q

path of facial nerve motor nerve

A

from lateral brain
cerebellopontine angle
internal auditory meatus
facial canal
exit through stylomastoid foramen

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31
Q

path of parasympathetic fibers of facial nerve

A

With facial nerve into internal auditory meatus

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32
Q

what part of tongue is innervated by the facial nerve?

A

anterior 2/3

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33
Q

what is bells palsy

A

acute paralysis of the face related to a inflammation or swelling. usually unilateral.

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34
Q

etiology of bells palsy

A

idiopathic
Herpes zoster (Ramsay Hunt syndrome)
HSV reactivation
Borreliosis (Lyme disease)
Diabetes mellitus

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35
Q

what is bells phenomenon

A

attempt to close eyes and show teeth one eye can’t close and eyeball roles back

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36
Q

treat bells palsy

A

protect eye when sleeping + eyedrops
high dose prednisolone 10 days
antiviral therapy if known virus

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37
Q

Ramsay hunt syndrom

A

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

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38
Q

hemifacial spasm

A
  • unilateral clonic spasms from orbicularis occuli then to rest of face
  • contractions are irregular and increases with emotional stress and fatigue
  • cause: vascular comprssion of facial nerve at root entry zone like tumor
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39
Q

vertigo dizziness

A

loss of orientation of body in space
leads
to feeling that Room is spinning

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40
Q

causes of Central vertigo

A

■ Tumor (astrocytoma)
■ Cerebrovascular disorders
● Stroke
● Vertebrobasilar insufficiency
● TIA
■ Migrainous vertigo
■ Drugs/toxins
■ Multiple sclerosis (demyelination)
■ Inflammation (meningitis, cerebellar abscess)
■ Trauma

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41
Q

etiology of peripheral vertigo (85%)

A

■ Idiopathic
■ Menière’s
■ BPPV (benign paroxysmal positional vertigo)
■ Trauma
■ Drugs: streptomycin, quinine, salicylates
■ Labyrinthitis
■ Vestibular neuronitis
■ Cerebellopontine angle tumors
● Acoustic neuroma
● Meningioma

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42
Q

non-vertigo dizziness

A

Psychogenic (diagnosis of exclusion)
■ Depression
■ Anxiety etc

Vascular
■ Orthostatic hypotension
■ Arrhythmia
■ CHF
■ Aortic stenosis
■ Vagovagal episodes

Ocular
■ Decreased visual acuity

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43
Q

nystagmus in central vs peripheral nystagmus

A

central: Bidirectional horizontal or vertical
Peripheral: Unidirectional horizontal or rotatory

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44
Q

6 things you compare central vs peripheral

vertigo

A

imbalance
nausea vomiting
auditory symp
neurological sympt (diplopia, headache, dysphagia)
compensation (rapid in peripheral)
nystagmus

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45
Q

Ménière disease is a

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.

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46
Q

to differentiate vertigo from dizziness

A

vertigo: WORLD IS SPINNING
dizziness: unsteady or lightheaded

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47
Q

Plegia vs paresis

A

plegi: complete loss
paresis: loss of power

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48
Q

Different pareses/plegias

A

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,

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49
Q

Lesion of the corona radiata and the internal capsule causes

A

contralateral severe spastic hemiparesis

with involvement of the lower part of the face and the tongue

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50
Q

Isolated lesion of the corticospinal tract in the cerebral peduncle and lesion of the pyramid in the medulla cause

A

flaccid weakness,
however the joint lesion of all descending tracts leads to spastic hemiparesis.

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51
Q

Unilateral lesion of the base of the pons causes

A

contralateral hemiplegia/paresis, often sparing the face

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52
Q

Bilateral lesion of the base of the pons causes

A

quadriparesis/plegia.

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53
Q

Unilateral lesion of the cervical spinal cord at the level of C1-4 segments causes

A

ipsilateral spastic hemiparesis.

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54
Q

Bilateral lesion of the cervical spinal cord at the level of C1-4 segments causes

A

spastic quadriparesis

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55
Q

Lesion of the cervical spinal cord at the level of C5-Th1 segments causes

A

flaccid weakness of the upper limbs
spastic weakness of the lower limbs

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56
Q

Lesion of the thoracic spinal cord causes

A

spastic paraparesis

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57
Q

Lesion of the lumbosacral spinal cord causes

A

flaccid paraparesis.

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58
Q

Lesion of spinal motor neurons and anterior roots causes

A

flaccid weakness of segmental
distribution (in the corresponding myotomes)

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59
Q

Polyneuropathy typically causes

A

distal symmetrical flaccid weakness of the limbs, first on the lower limbs.

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60
Q

most important symptom of UMNL and LMNL

A

UMNL: BABINSKY - positive pyramidal sign
LMNL: visible fasciculation’s

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61
Q

lateral corticospinal tract is for

A

distal limbs and fine manipulation

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62
Q

anterior/ventral corticospinal tract is for

A

trunk and upper leg muscles (posture locomotor)

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63
Q

UMNL paralysis:
LMNL paralysis:

A

UMNL paralysis: spastic
LMNL paralysis: flaccid

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64
Q

spasmicity vs rigidity

A

Spasticity: resistance in one direction. Velocity-dependent.
Rigidity: resistance in all directions. Not velocity-dependent

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65
Q

fasciculation vs fibrillations

A

○ 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

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66
Q

main cause of UMNL

A

stroke
demyelination
ALS(Amyotrophic lateral sclerosis )

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67
Q

main cause of LMNL

A

polio
west nail virus
spinomuscular athropy (SMA)
cauda eq. syndrom
DM neuropathy
botulism
ALS

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68
Q

what are the two fibers innervated in a muscle

A

Intrafusal Gamma fibers: reflex
Extrafusal alpha fibers contraction

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69
Q

where does the corticospinal tract deccusate

A

in the pyramids (brainstem)

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70
Q

what is the cerebrobulbar tract?

A

goes from cortex to pons/medulla and innervate CN

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71
Q

destination of corticobulbar tract

A

CN 5
CN 7
Nucleus ambiguous: CN 9, 10, 11
CN 12

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72
Q

why is there atrophy in UMNL

A

loss of usage
loss of Ach release causing no AP or protein synthesis,
80% muscle loss

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73
Q

pathophysiology of fasciculations?

A

no Ach causes increase in R formation and increased mechanical sensitivity - tapping causes activation of receptors opening Na channels and AP

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74
Q

why is there spasmic paralysis in UMNL

A

because of less inhibitory signals from medullary reticulospinal tract causing hyperflexia and hypertonia

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75
Q

which side is the speech scenter on?

A

LEFT hemisphere is dominant in most people

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76
Q

what is aphasia

A

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

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77
Q

Broca’s and Werncks aphasia is?

A

Broca: Expressive
Wernicks: receptive

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78
Q

Areas in Brocas

A

BA 44
BA 45

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79
Q

areas in wernicks

A

WA 22
WA 39
WA 40

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80
Q

BA aphasia present?

A

know what do say but cant say it
NON FLUENT
(understand but can’t find words)
skjønner men finner ikke ord

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81
Q

WA aphasia present?

A

difficulty understanding and finding right words, mix up words
snakker om helt rare ting

FLEUNCY INTACT
problem with comprehension and repetion

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82
Q

causes of aphasi

A

stroke
trauma
brain mass
neurodegenerativ disorders
encephalitis

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83
Q

conduction aphasia

A

understands and speaks but cant repeat

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84
Q

what supplies speech area?

A

middle cerebral artery

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85
Q

which artery infarct causes wernicks aphasia?

A

BRANCH OF MIDDLE CEREBRAL ARTERY: posterior temporal artery

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86
Q

etiology of conduction aphasia

A

Lesion of the arcuate fasciculus.
Characterized by normal speech,
but impaired repetition.
Patient is aware and frustrated by this.

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87
Q

alexia without agraphia

A

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)

alexia=inability to read or comprehend written language

agraphia= loss of a previous ability to write

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88
Q

how can you find out which side language center is on?

A

dominant hand: right hand - left area
left hand: mix of both 70% left 15% right 15% bilateral

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89
Q

what connect BA and WE

A

arcuate nucleus

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90
Q

The anatomical basis of arousal is the

A

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

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91
Q

Disorder of arousal

A

● 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

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92
Q

disorders of awakefullness

A

akinetic mutism (decorticate state)
confusion
delirium
Persistent vegetativ state
locked in syndrom (not disorder of conciousness but often misdiagnosed as this)

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93
Q

define persistant vegetativ state

A

Awake but no awareness of their surroundings.
Rostral brainstem remains intact → Thermoregulation (hypothalamus), sleep-wake cycle, endocrine system, cardiorespiratory and other visceral functions are intact

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94
Q

when is a vegetativ state permanent?

A

> 30 days

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95
Q

decorticated position

A

stiff with bent arms, clenched fists, and legs held out straight. Sign of severe damage in the brain

lesion above RN in proximal brainstem; loss of the inhibition of RN from higher brain centers > RST causes flexion of UE
also loss of inhibition of VN causes extension of LE

betterprognosis than decerebrate

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96
Q

decerebrated position

A

all limbs are stiff en extended.
Results from injury at distal brain stem or pons lesion ( at level or below RN; flexors not working)

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)

overactive VST

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97
Q

causes of vegetativ state

A

○ Extensive white matter damage
○ Bilateral damage to the thalamus
○ 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)

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98
Q

define akinetic mutism

A
  • Awake, but mute and does not move.
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99
Q

Etiology of akinetic mutism

A

Caused by bilateral interruption of connections between the supplementary motor area,
cingular region and
midline nuclei of the thalamus

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100
Q

are you paralised in akinetic mutism

A

NO, because of withdrawal reflex to pain, suckling reflex, and grasp reflex

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101
Q

what can cause akinetic mutism

A

○ Jet bleeding (ruptured Ant. communicating a. aneurism)
○ Bilateral ischemia in the anterior cerebral artery
○ Subfalcial/cingulate herniation
○ Occlusive hydrocephalus
○ Butterfly tumors growing across the corpus callosum
○ Tumors of third ventricle

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102
Q

define delirium

A

Cannot focus, change or fix attention.
Disoriented and incoherent thinking.
evolves over 24h.
inversion of sleep wake cycle. sweating, tachycardia unstable BP

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103
Q

what do you have to have to be counscious`

A

awareness
arousal
alertness
memory

AAAM

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104
Q

function of ascending reticuloactivating system (ARAS)

A

reflexes
sensory information
respiration
HR/BP
sleep cycle
consciousness
posture

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105
Q

composition of ARAS system?

A

medial column
lateral column
median column
composed of A LOT of nuclei

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106
Q

4 things to look for first in an unconscious patient

A

looks like sleeping?
spontaneous movement?
respons to voice/stimuli?
respiration stable?

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107
Q

how do you examine a uncounscious patient?

A
  1. observe
  2. stabile ABC
  3. GCS
  4. signs of external Trauma
  5. eye position and reflexes
  6. limb position and reflexes
  7. deep tendon reflex
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108
Q

GCS values

A

< 3 high rate of death
< 8 coma –> intubate
15 is normal

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109
Q

deep tendon reflexes?

A

There are five primary deep tendon reflexes:
biceps, brachioradialis,
triceps, patellar, and ankle.

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110
Q

brain stem reflexes

A

Pupillary Light Reflex.
Corneal Reflex
Oculo-vestibular Reflex
Pain Stimulus.
Gag Reflex.
Cough Reflex.

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111
Q

findings in an unconscious patient and their cause?
ocular symptoms:
1. Pupillary constriction (light reactions are preserved!)
2. Pupillary dilation (NO pupillary light reactions)
3. Fixed, moderately dilated pupils

Gaze disorders
4. Skew deviation (eyes diverge in vertical direction, one down, the other up)
5. Persistent upward deviation
6. Persistent downward deviation

A
  1. Bilateral → hypothalamus and diencephalon damage. Unilateral: Horner’s
  2. tectum lesions
  3. lesion below tectum
  4. caudal part of brainstem and meso-diencephalon damage
  5. global cerebral ischemia
  6. hepatic coma
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112
Q

what are the two vestibular reflexes

A
  1. Vestibulo–ocular reflex: move head side to side, pupils should move in opposite direction.
  2. caloric reflex: cold/warm water stimulus COWS, a test of vestibuloocular reflex
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113
Q

what type of unconsciousness is normally related to metabolic origin?

A

persistent vegetativ state also called unresponsive awakefullness syndrom

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114
Q

metabolic causes of unconsciousness

A

● 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

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115
Q

how can you diff between structural defect or coma due to hypoglycemia?

A

pupillary reflex normally intact if hypoglycemia

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116
Q

what glucose level causes coma?

A

< 0.6 mmol/L

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117
Q

what is seen in hyperglycemia

A

hyperosmolar effect can cause coma. Can cause involuntary movements, seizures and hemiparesis

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118
Q

symptomes in ketoacidosis

A

Symptoms: dehydration (due to osmotic diuresis), fatigue, weakness, headache, abdominal pain,
Kussmal breathing, confusion, coma

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119
Q

when is consciousness lost if pO2 drops

A

< 40 mmHg

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120
Q

pupils in hypoxia?

A

large and reactive

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121
Q

9. Unconsciousness due to metabolic origin

what happens in renal/uremic encephalopathy`

A

false neurotransmitters in brain like Octopamine.
imbalance between excitatory and inhibitory
EEG shows slow waves

A sign of acute renal failure
● Brain amino acid metabolism is also impaired, and causes an imbalance between excitatory and
inhibitory neurotransmitters or accumulation of false neurotransmitters

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122
Q

symptoms hepatic encephalopathy

A

pupils small-reactive
Asterixis,
myoclonus, dysarthria, ataxia,
hyperreflexia,
hemiparesis

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123
Q

define
Myoclonus
Dysarthria
ataxia

A

Myoclonus: uncontrolled jerking
Dysarthria: speech muscle weakness
ataxia: loss of limb muscle control

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124
Q

glucose level in hyperosmolar hyperglycemia`

A

VERY VERY high - monitor cant read > 600 mg/d

(>33.3 mmol/L)

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125
Q

treatment of HHS

A

0.9% saline then 0.45%
change to dextrose when glucose is 250 mg/d (13.9 mmol/L)
give regular insulin IV OBS K+ must be > 3.3

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126
Q

what electrolyte disturbance causes coma

A

Hyper Na / Hypo Na
Hyper Cl /hypo Cl
Hyper Mg
Hypo K+ / Hyper K+

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127
Q

drug intoxication causing coma

A

overdose in suicidal intent of sleeping pills and sedativs

128
Q

areas most sensitiv to hypoxia

A

basal ganglia and cortex, hippocampus, brainstem

  • grey matter more vulnerable than white
129
Q

neurological states causing resp failure

A

The CNS → Raised ICP - hernia
The PNS → Myasthenia, Guillan-Barré syndrom

130
Q

3 causes of an neurological emergency

A
  1. stroke
  2. seizure
  3. unconsciousness
131
Q

what are the 3 main components of intracranial volume?

A

CSF
brain tissue
Blood
if one increase the other must decrease

132
Q

CSF volume

A

approximately 125 mL to 150 mL

133
Q

normal intracranial pressure

A

7–15 mm Hg

134
Q

monroe Kellie principle

A

cerebral bloodflow is the ratio of CAP and CVP (AP/VP) = cerebral perfusion pressure
IC pressure = CVP
so increase in ICP always increase CVP thus decrease perfusion pe

CPP= MAP - ICP (or CVP)

135
Q

what are the two principle ways of decreasing ICP

A

by decreasing CSF (physiological)
by decreasing blood (not physiological)

136
Q

how can we decrease BF to brain?

A

Hyperventilation dec. CO2 and causes capillary restriction and decreased CVP
Barbiturate narcosis decreases metabolism need
Hypothermia decreases metabolism need

137
Q

causes of increased ICP

A
  1. Space-occupying lesions (eg. tumor, abscess, hemorrhage) - treat with surgery
  2. CSF disorders (occlusive hydrocephalus) - treat with CSF drainage
  3. Cerebral edema (vasogenic, cytotoxic, interstitial)
138
Q

clinical presentation of increased ICP

A

● Progressive headache (one of leading complaints)
● Vomiting
● Papilloedema + blurred vision
● Always global cerebral dysfunction due to global cerebral ischemia

139
Q

treatment of high ICP

A

● Treat underlying etiology
● Osmodiuretics (mannitol, glycerol)
● Loop diuretics decrease CSF production
● ICU:
○ Controlled hyperventilation
○ Barbiturate narcosis
● Decompressive craniectomy

140
Q

how can you pres CSF out of head yourself?

A

valsava manuver

141
Q

what are the 4 brain herniations?

A
  1. Cingular/subfalcial
  2. central
  3. transtentorial
  4. transforaminal/tonsillar
142
Q

what happens in Cingular/subfalcial herniation

A

Cingular gyrus in pressed under the falx.
May compress circumferential branches of anterior
cerebral artery (pericallosal, collosomarginal) if mass
effect is considerable.

143
Q

what happens in central hernia

A

Compression of diencephalon.
Severity is proportional to lateral or axial shift of diencephalon.

144
Q

what happens in transtentorial hernia

A

Compression of mesencephalon “Midbrain” in tentorial incisure -
* damaged blood supply of mesencephalon
and
* secondary intraparenchymal bleedings.

145
Q

which artery bleeds in
epidural
subdural
subarachnoid

A
  1. MCA
  2. bridging veins
  3. intracranial aneurism rupture
146
Q

what to asses on a intracranial injury

A

○ Period of loss of consciousness: relates to severity of diffuse brain damage
○ Period of post-traumatic amnesia: reflects severity of damage
○ Period of retrograde amnesia
○ Cause and circumstances of the injury: e.g. epilepsy
○ Presence of headache and vomiting: if they persists, IC hematoma must be considered

147
Q

imaging in IC hematoma suspicion

A

stat CT !!

as soon as possible

148
Q

symptomes indicating specific locations of basal skull fractures

A

○ Anterior fossa fracture:
* CSF rhinorrhea (contains glucose),
* bilateral periorbital hematoma,
* subconjunctival hemorrhage
* Raccoon eyes: subcutaneous hematoma around the eyes

○ Petrous fracture:
* bleeding from external auditory meatus or CSF otorrhea,
* subcutaneous hematoma/ bruising over the mastoid (Battle’s sign)

149
Q

management of intracranial hematoma

A

Extradural: horseshoe craniotomy flap
w/ complete evacuation of the hematoma

Subdural/intracerebral: question mark flap over temporal and/or frontal areas
w/
subdural/intracerebral evacuation of hematoma and necrotic brain

150
Q

IC bleeding pattern on imaging

A

Epidural is lens shaped
subdural cresent shaped

151
Q

outcome of acute transvers spinal cord injury

A

quadriplegia
anesthesia
loss of all function below injury site

152
Q

Brown-Sequard syndrom

A
  • Rare, mainly due to trauma (e.g. gunshot, stabwound)
  • Ipsilateral proprioceptive sensory loss
    (proprioceptive tract) and weakness (corticospinal tract)
  • with contralateral loss of pain and temperature (spinothalamic tract)
153
Q

central spinal cord syndrom presentation

A

Hyperextension injury
-arm weakness
-sensory deficit (pain,temp)
-motor deficit

Lateral CS stract: cervical+thoracic
White commissure: pain, T, crude touch
anterior grey horn LMNL

154
Q

posterior spinal cord lesion

A

Dorsal column: gracilis, cuneate: proprioception, vibration, disc. touch

155
Q

anterior spinal cord lesion

A

anterior 2/3 are involved
autonomic fibers: incontinence
Corticospinal tract: UMNL
Anterior grey horn LMNL
spinothalamic tract: pain, temp, crude touch
only preserved is the dorsal column

complete motor paralysis
loss of pain temp feeling below injury

ASA

156
Q

conus medullaris syndrom

A

between T12-L1 (BBI)
back pain
Bilat sensory loss
Incontinence

Sensory loss (numbness) in the perianal region and inner thighs (saddle anesthesia) and
loss of bladder control (retention with overflow incontinence)
without leg weakness or diminished stretch reflexes

157
Q

Cauda equina syndrome

A

belowL2

Lumbosarcal Radicular pain in several dermatomes,
flaccid paralysis of lower limbs with loss of deep tendon reflexes and
overflow incontinence
saddle anesthesia: loss of sensitivity at dermatomes s3-s5

158
Q

jefferson vertebrate fracture

A

fracture of both arches of C1
stiff neck, pain when moving, no neuro signs

159
Q

Dens vertebrate fracture

A

C2 fracture
Neck pain radiating to occipital region (worse with neck movements), typically the patient
will hold their head

160
Q

type A C B vertebrate fractures

A

A: compression = shortening
B: distraction = lengthening
C: Torsonal = rotation (shearing force)

161
Q

symptoms of impaired circulation of ICA

A

○ Deterioration of consciousness
○ Homonymous hemianopia of the c/l side
○ Contralat hemiplegia
○ Contralat hemisensory disturbance
○ Gaze palsy to opposite side, eyes deviated to the side of lesion
● A partial Horner’s sy. may develop (SY fibers on the ICA wall)
● Occlusion of the dominant hemisphere → global aphasia

162
Q

Occlusion of anterior cerebral artery

A

supplies medial part of hemisphere: lower limb
primary motor cortex:
* contralateral weakness

somatosensory cortex:
* contralateral sensory loss

163
Q

occlusion of middle cerebral artery

A

supply lateral part of hemisphere: upper limb

sensory and motor loss + Broca’s area

164
Q

occlusion of posterior cerebral artery

A

Occipital lobe: vision
homonymous hemianopia

165
Q

what does insula do

A

decision-making

166
Q

supplied by the vertebrate arteries

A

medulla and inferior surface of cerebellum

167
Q

supplied by the basilar artery

A

brain stem from medulla and up and gives off PICA and AICA

168
Q

what is supplied by the vertebrobasilar system

A

brainstem, midbrain, pons , medulla
, cerebellum, occipital lobe, , thalamus

169
Q

symptoms of vertebrobasilar insufficiency

A

○ Drop attacks (weakness of quads→ fall to the ground)
○ Diplopia
○ Dysarthria
○ Dizziness
○ Vertigo
○ Dysphagia

resolves within 24h

170
Q

cause of vertebrobasilar insufficiency

A

VBI is usually caused by
atherosclerosis, hypertension,
diabetes, smoking, dyslipidemias.

171
Q

how to treat VBI

A

Treatment often includes lifestyle changes and treatment of underlying conditions.

Patients can also get started on antiplatelet or anticoagulation.

Angioplasty is a possibility

172
Q

posterior cerebral artery stroke

A
  • Contralateral hemianopia or quadrantanopia
  • Midbrain findings:
    -ipsilateral CN3 III and CN4 IV palsy/pupillary changes,
    -contralateral hemiparesis/hemiplegia (= Weber’s syndrome)
  • Posterior cortical infarction in dominant hemisphere: problems in naming colors and
    objects
173
Q

basilar artery stroke

A

locked in syndrom
- bilateral loss of corticospinal tract - complete paralysis
- Preserved vertical eyemovement + blinking
- patient is conscious alert and aware

174
Q

AICA stroke

A

lateral pontine syndrome
- I/L CN VII facial n palsy
- I/L vestibular nuclei damage: vertigo and nystagmus
- I/L Ataxia: poor coordination

  • C/L loss of pain and temp (ST tract)
175
Q

anterior spinal artery stroke

A

Causes medial medullary infarct
○ Contralateral hemiparesis (facial sparing),
contralateral impaired proprioception and vibration,
* ipsilateral tongue weakness

176
Q

PICA stroke

A

loss of coordination, balance and muscle tone
CN X - dysphagia and loss of gag reflex
horners syndrom

177
Q

what is horners syndrom

A

ptosis
miosis
anhydrosis

178
Q

occurrence of ischemic vs hemorrhagic stroke?

A

ischemic 85%
hemorrhagic 15%

179
Q

what is a ischemic stroke tat resolves within 24h called?

A

TIA

180
Q

causes of ischemic stroke?

A

endothelial; clotting
embolism/thrombosis

-atherosclerosis: stenosis, occlusion
-dissection
-vasculitis
- emboli
- lacunar occlusion of small vessels

can transform to hemmorhagic after few days (common in cardioembolic stroke)

181
Q

first imaging in a ischemic attach

A

stat CT no contrast to rule our SAH or ICH

182
Q

if no SAH or ICH and you cant see lesion on CT you…

A

take a CT angio and look for filling defect

183
Q

MRI on a ischemic stroke you do

A

DWI and PWI are compared, if hypoperfusion seen > thrombolysis

DWI and a ADC and compare them
DWI show bright hyperintens
ADC show dark hypointens

Apparent diffusion coefficient

184
Q

treatment of ischemic stroke

A
  1. last known well < 4.5h ago give TPA
  2. if last known well is more then 4.5-6h ago evaluate:
    - no SAH/ICD
    - no hypoglycemia or previous stroke
    - NIHSS < 25
    - infarct is < 1/3 of MCA territory
185
Q

contraindication of TPA

A

If the ischemic stroke is affecting >⅓ of the MCA territory - reperfusion can lead to hemorrhagic transformation
○ Mild symptoms/symptoms improving
○ Cerebral trauma or AMI in the last 3 months
○ Surgery the last 2 weeks
○ Present or previous intracranial hemorrhage/SAH
○ BP >185/110 mmHg
○ Peptic ulcer, epilepsy, hypoglycemia, fracture
○ INR>1.7, abnormal APTT, PLT<100.000/mm3

186
Q

what to do if no tpa treatment in stroke

A

mechanical thrombectomy
if large vessel occlusion MCA, ICA, Basilar
-endovascular thrombectomy within 6hrs of onset of symptoms

-intraarterial thrombolysis : within 6 hrs

187
Q

BP goals in stroke

A

if tPA < 185
if no tPA < 220

188
Q

BP medication in stroke

A

NIcardipin IV
Labetolol IV
Hydralazine

189
Q

DOAC’s
Direct oral anticoagulants

A

dabigatran (direct thrombin (factor IIa) inhibitor)
rivaroxaban ( factor Xa inhibitors.)
apixaban (Xa inhibitors)

190
Q

most common cause if hemorrhagicc stroke

A

sustained HT causing rupture
trauma
cerebral amyloid angiopathy (b-amyloid plaque)
coagulopathy
hemorrhagic transformation from a ischemic stroke
malignancy

191
Q

most common location of a hemorrhagic stroke

A

pons
cerebellum
basal ganglia
thalamus
cortex (least common)

192
Q

what to look for on imaging in hemorrhagic stroke ICH

A

midline shift
hydrocephalus/IVH

Expansion of the hematoma displaces the cortex outward, causing edema in the surrounding area within hours of the initial hemorrhage. This leads to mass effect on other structures, such as the ventricles, which may result in hydrocephalus. Sulci may appear compressed, with the gyri expanded and flattened.

193
Q

blood pressure goal im hemorrhagic stroke

A

140/90 mm Hg
and if possible and tolerable to 130/80 mm Hg or even lower

194
Q

reversal of anticoagulants

A

warfarin - vit K
Heparin - protamin
Dabigatran -Idarucizumab (monoclonal Ab)
Apixaban or Rivaroxaban- Andexanet alfa = recombinant modified human factor Xa

195
Q

when to intubate in cerebrovascular disorders

A

intubation is necessary if bulbar reflexes are absent/patient is in coma

196
Q

when to mechanical ventilate in cerebrovascular disorders

A

saturation < 90% or pCO2 > 50 mmHg → mechanical ventilation

197
Q

give glucose in cerebral ischemia?

A

Glucose is contraindicated in cerebral ischemia (except in hypoglycemia).

198
Q

when to give insulin?

A

Insulin should be given if glucose levels > 15 mmol/L (target: 7,8-10 mmol/L

199
Q

nucleus related to dysphagia

A

nucleus ambignous

200
Q

dose of tPA

A

0.9 mg/kg (max 90mg), and 10% is given as i.v. bolus followed by 1h infusion of remaining 90%. Check BP and neurologic symptoms every 15 min during infusion.

201
Q

when is follow up CT indicated in stroke

A

24h

202
Q

when should antiplatelet therapy start in stroke

A

NOT before 24h

203
Q

define cerebrovascular disorder

A

Cerebrovascular disorders include all disorders in which an area of the brain is temporarily or
permanently affected by ischemia or hemorrhage, and one or more of the cerebral blood vessels are
involved in the pathological process.

204
Q

stroke Protocall

A
  1. ABCDE (remember glucose)
  2. Blood samples (Glucose, INR) and blood pressure
  3. GCS, NIHSS: neurological screening assessment
  4. ECG (should not delay CT/MRI)
  5. CT or MRI (should be interpreted within 45 minutes)
    ○ Hemorrhage: consult neurosurgeon
    ○ Ischemia: candidate for thrombolysis
  6. Thrombolysis (rtPA) if within therapeutic window
205
Q

how can imaging tell us if we are still in the therapeutic window?

A

DWI shows ischemia while FLAIR shows no ischemia

206
Q

how can imaging show if there is pneumbra?

A

DWI-PWI mismatch: DWI shows infarct core, while PWI shows hypoperfused tissue,

207
Q

INR value allowing thrombolysis ?

A

< 1.7

208
Q

mandatory to check before thrombolysis

A

● Hypoglycemia (glucose): can mimic acute stroke
● Coagulopathies (INR): CI of thrombolysis (should be under 1,7 to perform)
● Blood pressure (BP): hypertension increase hemorrhagic risk of thrombolysis

209
Q

diagnostic considerations in cerebrovascular disease

A

Presence of clinical signs (WHO)
● Hemorrhagic vs. ischemic (CT, MRI)
● Pathomechanism (thrombotic, embolic, hemodynamic, small vessel disease)
● Duration of signs
● Brain region (hemisphere, cerebellum, brainstem; territorial-borderzone)
● Anterior-Posterior
● Supplying vessel (carotid artery, vertebrobasilar, lacunar, ACA, MCA, PCA)
● Prognostic by signs (Bamford – OCSP)
○ TACI, PACI, POCI, LAC

Total anterior circulation infarct (TACI
partial anterior
Posterior circulation infarct
Lacunar stroke

210
Q

○ TACI, PACI, POCI, LAC

A

TACI: total anterior circulatory stroke
PACI: partial anterior circulatory stroke
POCI: posterior circulatory syndrom
LACI: Lacunar syndrom

211
Q

cranial nerves run in the cavernous sinus what can happen

A

oculomotor
Opthalmic
maxillary
abducent
can be compressed if infection causing CN palsy

212
Q

eye innervation muscle

A

superior, medial and inferior rectus + inferior bliq by CN III
lateral rectus by CN VI
superior oblique by CN IV

213
Q

2 venous systems of brain

A

superficial and deep + sinuses

214
Q

Thrombotic occlusion of the venous system occurs with:

A

● Infection (especially ear or sinus infection)
● Dehydration
● Pregnancy and puerperium
● Coagulation disorders
● Malignant meningitis
● Miscellaneous disorders (e.g. sarcoid, Behçets)

215
Q

most frequent place of venous thrombosis in brain

A

Superior sagittal and lateral sinus thrombosis (85% of cases)

216
Q

symptoms of cerebral venous thrombosis

A

○ Impaired CSF drainage results in headache, papilloedema and impaired consciousness.
○ Venous infarction produces seizures and focal deficits (e.g. hemiplegia).

217
Q

CT sign of venous thrombosis

A

(Δ) ‘Empty delta’ sign
Consists of a
* central hypodensity (representing the thrombus)
* with a triangular outline of contrast enhancement

May be seen in cerebral venous thrombosis of the superior sagittal sinus.

(contrast filling defect: following contrast the wall of the sinus enhances but not the central thrombus on CT)

218
Q

treatment of cerebral venous thrombosis

A

Treatment: Correct causative factors (dehydration/infection etc.) + anticoagulation with heparin or alternative

219
Q

cavernous sinus thrombosis signs

A

● Commonly results from infection from the jaw
● Painful ophthalmoplegia, proptosis and oedema of periorbital structures are associated with facial numbness and fever.
● The disorder may be bilateral.
● Treatment with antibiotics and if indicated, sinus drainage.

ophthalmoplegia, paralysis of the extraocular muscles that control the movements of the eye.

220
Q

prognosis of intracranial bleedings?

A

approximately half of patients
die within 30 days

221
Q

most common site of intracranial bleeding

A

In hypertensive patients 70% occur in the basal ganglia/thalamic region. In normotensive patients, 37% occur in this area

222
Q

signs of intracerebral hemorrhage

A
  1. Basal ganglia - Hemiparesis, sensory loss, eye deviation
  2. Thalamus - Sensory loss, later hemiparesis, gaze disturbance
  3. Lobar - Better prognosis, intraventricular bleeding is rare
  4. Cerebellar - Nausea, ataxia, dizziness, signs of brainstem compression (30% mortality)
  5. Pons - Fast progressing hemi- or tetraparesis, disturbed eye movements, decerebration, small
    pupils, disturbance of breathing, coma, death (high mortality
223
Q

pathological effect of intracerebral hemorrhage

A

● Space-occupying effect → Brain shift
● Continued bleeding → Expanding may continue beyond the first few hours.
● Within 48 hours: disruption of BBB, vasogenic and cytotoxic edema, neuronal damage and necrosis
● Resolution in 4-8 weeks → Cystic cavity

224
Q

complication of intracerebral hemorrhage

A

● Repeat hemorrhage
● Vasospasms
● Deep vein thrombosis
● Dysphagia (can lead to aspiration pneumonia)
● Elevated ICP → Brain herniation
● Seizures
● Hydrocephalus
● SIADH

225
Q

caus of SAH

A

Traumatic brain injury can cause aneurism
Non-traumatic:
● Aneurysms (75%) rupture
● perimesencephalic hemorrhage (10%),
● Ruptured arteriovenous malformations (AVM) (5%)

● Others: cortical thrombosis, angioma, neoplasm, infection
● 20% of investigations fail to reveal the source
* triggered by acute increase in BP

226
Q

signs and symptomes of SAH

A

Signs and symptoms
● Severe headache w/ instantaneous onset
● Loss of consciousness, coma
● Epileptic seizure
● Nausea, vomiting
● Neck stiffness present in most pts
● Focal signs (e.g. limb weakness, dysphasia)
● Reactive hypertension
● fever

227
Q

diagnosis of SAH

A

● Urgent CT without contrast: detects 95% of SAH within 24h
● Lumbar puncture: if CT is neg. but history is very suggestive of SAH,
needs to be done >12h after headache onset to allow breakdown of RBCs → a pos. sample is xanthrochromic (yellow due to bilirubin)
● MRI: may be used in pts w/ multiple aneurysms
● CT/MR angiography, digital angiography: more detailed info

228
Q

treatment of SAH

A

● Re-examine CNS often (BP, pupils, GCS)
● Maintain cerebral perfusion by keeping well hydrated (aim for SBP<160 mmHg)
● Nimodipine to prevent vasospasms
● Surgery: within 48h, if not a delayed intervention is recommended (after 14 days)
- surgical clipping, endovascular coiling.
- balloon remodeling and flow diversion (newer technique) to close aneurism

229
Q

aneurism surgery?

A

Endovascular coiling vs. surgical clipping, depending on accessibility and size of aneurysm (coiling is preferred)
Balloon remodelling and flow diversion are newer techniques used for anatomically challenging aneurysms

230
Q

define status epilepticus

A

A state of continuous seizure lasting ≥ 5 min, or ≥ 2 repetitive, separate seizures with consciousness not fully regained in the interictal period.

231
Q

what is epilepsy

A

Epilepsy: a chronic neurologic disorder characterized by a predisposition to seizures

232
Q

Generalized tonic–clonic seizure

A

A generalized tonic–clonic seizure, commonly known as a grand mal seizure, produces bilateral, convulsive tonic and clonic muscle contractions.

233
Q

Focal seizures

A

are seizures which affect initially only one hemisphere of the brain.

234
Q

Pediatric absence seizures

A

(also called petit mal seizures) are characterized by a brief altered state of consciousness and staring episodes. And do not cause your child to fall or have significant shaking movements.

235
Q

4 stages of a seizure

A

Prodromal.
Early ictal (the “aura”)
Ictal.
Postictal.

236
Q

how is the postictal stage after a seizure

A

Period that begins when a seizure subsides and ends when the patient returns to baseline.
It typically lasts between 5 and 30 minutes and is
characterized by disorienting symptoms such as
confusion, drowsiness, hypertension, headache, nausea, etc

237
Q

causes of seizure in adults

A

○ Antiepileptic drug withdrawal
○ Acute cerebral embolization
○ Metabolic disorder
○ Alcohol intoxication
○ Tumor
○ Neuroinfection

238
Q

causes of seizure in children

A

fever
infection

239
Q

what can confirm the end of status epilepticus

A

The termination of status epilepticus must be confirmed by EEG (due to non-convulsive or
electrographic status epilepticus)

240
Q

why must treatment in status epilepticus happen fast

A

The risk of a focal status epilepticus turning in to a generalized one is relatively high, therefore
treatment is similar in both forms

241
Q

treatment in status epilepticus

A

0-5 min usually self limeting do ABCDE, IV accsess, glucose

5-20 min give midazolam IM 10mg or lorazepam IV 0.1mg/kg or diazepam

20-40 min fosphenytoin, Valproic acid IV , levetiracetam

40-60 min repeat 2nd line therapy Valproic
- anesthetic doses of midazolam or thiopental (with continuous EEG)

242
Q

etiology of viral meningitis

A

○ 80% is caused by enteroviruses (coxsackie, echo, nonparalytic polio).
○ Less commonly caused by VZV, HIV, mumps.
○ Outbreaks are especially common in early spring and late autum

243
Q

etiology of bacterial meningitis

A

○ Most common pathogens: pneumococcus pneumoniae, N. meningitidis, Listeria (mostly
in alcoholics or when using systemic immunosuppressants)
○ In childhood Staphylococci are the most common pathogens.

244
Q

why can pathogens proliferate easy in the brain

A

The primary immune response in the CNS is weak, as there is no MHC I and II antigens on
neurons or astrocytes; thus they are not able to do phagocytosis

245
Q

most common rout of infection to meninges in meningitis

A

Most common route of infection: colonization in nasopharynx → subdural space → subarachnoid
space → meninges and basal cisterns (meningeal signs

246
Q

Clinical signs and complications of meningitis

A

● Nuchal rigidity, meningeal signs and altered consciousness
● In case of N. meningitidis infection a petechiae can develop
● Serous or purulent exudate block absorption or circulation of CSF → hydrocephalus, cranial nerve abnormalities and altered consciousness
● Increased ICP due to vasogenic edema because of increased permeability of BBB

● Exudates in venous sinuses → thrombosis, reactive vasculitis and brain ischemia
● Ventriculitis when infection reaches the sinuses
● Bacterial: no AB treatment can lead to death in less than 24h. Prophylaxis is given to close contacts

247
Q

diagnosis of bacterial meningitis

A

Fluid: cloudy, unclear
Protein: high >1g/l
Lactate: high
Glucose: low >0.4 csf/sera
Cell count: High - leukocyte count > 1000/mm3
↑ Granulocytes (> 80%)
Do ELISA (or PCR for listeria)

248
Q

diagnosis of viral meningitis

A

Fluid: clear
Protein: norm
Lactate: norm
Glucose: norm
Cell count: Variable cell count (leukocyte 100–500/mm3)
↑ Lymphocytes
Do PCR

249
Q

meningitis treatment

A

● Empirical treatment with 3rd generation cephalosporin + amoxicillin + vancomycin i.v. should
be administered before culture results are ready
● Confirmed N. meningitidis: ciprofloxacin given to close contacts
● Viral: symptomatic treatment

250
Q

define encephalitis

A

Encephalitis: inflammation of the brain parenchyma

251
Q

etiology of infectious encephalitis

A

Arboviruses are the most common
Most common causative agents:
* HSV-1,
* VZV,
* tick-born encephalitis viruses
* Enterovirus spp.

In immunocompromised patients:
* CMV, JC viruses,
* Listeria, Mycobacterium, Mycoplasma spp

252
Q

what is limbic encephalitis

A

Limbic encephalitis: Antibodies against cell surface antigens such as receptors, e.g. anti-NMDA
receptor Ab mediated encephalitis (ovarian teratoma)

253
Q

define multiple sclerosis

A

A chronic progressive degenerative disease of the CNS characterized by demyelination and axonal degeneration in the brain and spinal cord, which are caused by an immune-mediated inflammatory processes

254
Q

type of reaction in MS

A

Type IV HS reaction - cell mediated

255
Q

pathophysiology of MS

A

Tcells are activated in periphery, then
cross react with parts of myelin in CNS leading to:
* demyelination
* secondary axon degeneration

attacks myelinproteins on nerve cells causing oligodendrocyte (CNS myelin) destruction and plaques called sclera - hence name multiple sclerosis - result is brain athropy

Inflammation and immune cell infiltration cause damage to the myelin, affecting the electrical signals moving along the neurons.

256
Q

types of MS

A

Plot neurological destruction up and time.
Relapsing-remitting (90%)
Secondary progressive
Primary progressive
Progressive relapsing

257
Q

in the CNS the only nerve with oligodendrocyte myelination

A

is the optic nerve causing optic neuritis

258
Q

symptomes on optic nerve because of MS

A

Optic neuritis:
loss of visual acuity : blurry vision

loss of color vision
afferent pupil defect - marcus gunn pupil - mydriasis

259
Q

what is seen in MS with eye movement

A
  • bilateral internuclear opthalmoplegia (brainstem symtpoms)

loss of connection between CN 6 and 3
when you look to the side only lateral movement works not medial by CN 3.
But if you ask the patient to focus on a pen it works

260
Q

diagnosis of MS

A

MRI:
periventricular lesions
brainstem lesions
SC lesions
Cerebellum lesions

CSF: oligoclonal gammopathy/bands = IgG Ab from plasma cells

VEP: decreased AP due to reduced conduction velocity
MEP, SEP - to detect subclinical lesions and predict course of disease

Serology (differential: borreliosis, treponema)

261
Q

treatmeant of MS

A
  1. high dose CS (methypredinisolone) OR
  2. Plasmapheresis
  3. Supportive:
    Spasmicity: Baclofen, dandrolone
    decrease detrusor hyperactivity: anticholinergic
    fatigue: amantidine
    paroxysmal symptoms: gabapentic, carbamazepine
  4. Disease modifying therapy to prevent relapses: (long term stability)
    Glatiramer acetate
    interferons
    Alemtuzumab (anti-cd52)
    Daclizumab (alpha intergrin; inhibits migration through BBB)
    Natalizumab (decrease relapse rate)

Autologous stem cell transplantation

262
Q

define brain edema

A

an excess of brain water, there’s three types of cerebral edema
a) Vasogenic
b) Cytotoxic
c) Interstitial

263
Q

define vasogenic edema

A

● Damage to the BBB → high protein content extracellular edema, spreading in white
matter along the nerve fibers
● Perifocal in tumors, central abscesses, parenchymal hemorrhage
generalized in meningoencephalitis
● Dx: T2-weighted MRI is most sensitive
● Tx: corticosteroids

264
Q

define cytotoxic brain edema

A

● Ion gradient btw the intra- and extracellular space decreases → Na+, Cl-, water moves into the neurons
→ damage to voltage-gated Ca++ ch.
→ Ca++ influx → fluid accumulates within cells
* ● Typical in cerebral ischemia in the area of cerebral cortex and basal ganglia, followed
by vasogenic edema as the capillaries are damaged
● Dx: diffusion-weighted MRI

265
Q

define interstitial edema

A

● Develops in occlusive hydrocephalus
● Increased CSF pressure → CSF pressed across ependymal layer of ventricles into the brain parenchyma

● Dx: hypodense halo surrounding the ventricles on CT,
high intensity signal on T2-weighted MRI

266
Q

treatment of brain edema

A

1) Causative treatment
2) Osmodiuretics (mannitol, glycerol)
3) Loop diuretics: decreases CSF production
4) Controlled hyperventilation: reduction of pCO2 by 10 mmHg decreases the ICP by 30% because of cerebral vasoconstriction
5) Barbiturate narcosis w/ EEG or plasma level monitoring
6) If ICP is so high that herniation is unavoidable → decompressive craniectomy
7) If occlusive hydrocephalus → temporary CSF drainage

raised ICP must be reduced!

267
Q

define wernick-korsakoff syndrom

A

Wernicke encephalopathy is an acute, reversible condition caused by severe thiamine (vitamin B1) deficiency, often due to chronic heavy alcohol use. Wernicke-Korsakoff syndrome is by definition when symptoms of two different conditions are seen
together; Wernicke´s Encephalopathy (WE) and Korsakoff Syndrome (KS).

268
Q

site of lesion in wernick-korsakoff syndrom

A

Lesions are bilateral around 3rd and 4th ventricle and the cerebral aqueduct.

269
Q

define Korsakoff syndrome

A

(chronic and only 20 % reversible with treatment): memory symptoms
- Anterograde amnesia (problems learning new information) and short-term memory loss
- Confabulations (make up information to fill memory gaps)
- Disorientation in time and space

270
Q

etiology of wenicks-korsakoff syndrome

A
  • Chronic alcoholism (most common)
  • Malnutrition (starvation, eating disorders, gastric surgery, cancer, prolonged vomiting etc) → decreased absorption of thiamine
271
Q

diagnosis of wernicks korsakoff syndrom

A

↓ Serum thiamine levels
↓ Erythrocyte transketolase activity (thiamine dependent)
↑ Serum lactate and pyruvate
Evidence of alcohol-related liver dysfunction

Brain MRI: T2-weighted hyperintense lesions
in the mammillary bodies,
midbrain tectal plate,
dorsomedial nuclei of the thalamus,
cerebellum,
and around the aqueduct and the third ventricle

272
Q

treatment of wernick korsakoff

A

Thiamine replacement iV
treat underlying condition

273
Q

Define Guillian-Barre

A

acute immune-mediated polyneuropathy that typically manifests with bilateral ascending flaccid paralysis and sensory involvement.

274
Q

coars of Gullian barre (GBS)

A

About two-thirds of GBS patients experience symptoms of an upper respiratory or gastrointestinal tract infection up to 6 weeks prior to onset of GBS.

275
Q

pathogens related to Gullian Bare Syndrome

A

Campylobacter jejuni: Campylobacter enteritis is the most common
Cytomegalovirus (CMV)
HIV
Influenza
Zika virus
Epstein-Barr virus
SARS-CoV-2
Mycoplasma pneumoniae

276
Q

pathophysiology of GBS

A

Postinfectious autoimmune reaction that generates cross-reactive antibodies (molecular mimicry)
Infection triggers humoral response → formation of autoantibodies against gangliosides

277
Q

diagnosis of GBS

A

CSF analysis:
May be normal in the first 1–2 weeks of the disease.
Typical: albuminocytologic dissociation (i.e., increased protein levels with normal leukocyte count < 10 cells/mcL in CSF)

Electromyography
Pathological spontaneous activity is a sign of an unfavorable prognosis.

278
Q

symptomes of GBS

A

Limb involvement:
Bilateral and ascending from the lower limbs
Progressive flaccid paresis or paralysis
Paresthesia (prikking): stocking‑glove distribution
Hyporeflexia typically begins in the lower limbs.

Back and limb pain (often an early symptom)
Involves nociceptive and neuropathic pain

Autonomic dysfunction
Cardiac arrhythmias, blood pressure fluctuations
Urinary retention and/or intestinal dysfunction

Respiratory muscle involvement may lead to respiratory failure.

Cranial nerve involvement
Facial palsy: due to bilateral facial nerve involvement (most frequently affected cranial nerve in GBS)

279
Q

treatment of GBS

A

IVIG or plasmapheresis

280
Q

define myasthenia gravis (MG)

A

Autoimmune disease of the neuromuscular junction (NMJ) characterized by muscle weakness that worsens with activity and improves with rest

281
Q

type of reaction in MG

A

Type 2 HS reaction - cytotoxic

282
Q

age distribution of MG

A

young women 20-30
Old men 60-70

283
Q

pathophysiology of MG

A

Responsible for inhibition of signal transduction at the neuromuscular junction (NMJ)
Antibodies target postsynaptic AChRs of normal muscle cells → competitive inhibition of acetylcholine (ACh) → AChR decay through receptor internalization (↓ receptor density at the postsynaptic membrane) and activation of complement (→ muscle cell lysis) → impaired signal transduction at the NMJ → skeletal muscle weakness and fatigue

284
Q

classification of MG

A

Ocular myasthenia: only the extraocular and/or eyelid muscles

Generalized myasthenia
All skeletal muscles may be involved.
Especially ocular, bulbar, limb, and respiratory muscles
- proximal limb weakness, hyperreactive reflexes.

bulbar form: dysarthia, dysphagia, myesthenic snarl (buccinator weakness produces characteristic smile)

285
Q

serotypes of MG

A

Seropositive MG (80–90% of cases): positive assays for antibodies (in blood) against the acetylcholine receptor (AChR-Ab)
Seronegative MG (10–20% of cases): negative for AChR positive for MuSK Ab (muscle specific kinase) , anti-striated muscle antibodies

286
Q

MG symptomes

A

Eye muscles: diplopia, blurred vision,ptosis
Bulbar muscles: dysarthria, difficulty chewing and/or swallowing
Proximal muscles: difficulty standing from a chair , climbing stairs, brushing hair
Respiratory muscles: dyspnea, respiratory failure

287
Q

MG diagnosis

A

● Clinical picture
● IV edrophonium = Cholinesterase Inhibitor (Tensilon) test: assess for improvement over 2 min, positive if clear
improvement in weakness

● Electromyography: Repetitive stimulation → decremental response (reduced amplitude)
● Serology: anti-AChR Ab (present in 70-90%), MuSK antibodies (30%)
● Chest CT/XR to screen for thymic hyperplasia (thymoma (10%) , persistent thymus (70%)

288
Q

MG treatment

A
  1. Cholinesterase inhibitor: first-line agent is pyridostigmine
  2. Immunosuppressants:CS, azathioprin
    Indications: inadequate symptom control with (or intolerance to) pyridostigmine
    -suppresses the production of antibodies
  3. Thymectomy if thymoma or severe generalised myesthenia
  4. Myesthenic crisis: IVIG / plasmapheresis
289
Q

diseases of micturition

A
  1. Spastic, neurogenic bladder
  2. Flaccid neurogenic bladder
  3. Detrusor-sphincter dyssynergia
  4. Frontal lobe incontinence
290
Q

Spastic, neurogenic bladder

A

CNS lesions above sacral spinal cord
→ Disinhibition and increased sensitivity (hyperreflexia) of detrusor muscle
→ Urge incontinence and decreased bladder capacity

291
Q

Detrusor-sphincter dyssynergia

A

● Uncoordinated function of detrusor muscle and external sphincter.
● Urge to urinate, but cannot due to sphincter spasm → Retention.
● From CNS lesions above sacral spinal cord. May have together with spastic bladder

292
Q

Flaccid neurogenic bladder

A

● Hypotonic bladder wall → Increased capacity.
● From lesion in sacral spinal micturition center (S2-4) or distally (conus, cauda equina, peripheral nerves).
● Bladder wall is insensitive and paralyzed → Overfilling → Overflow incontinence,
constant urine dripping

293
Q

Frontal lobe incontinence

A

● Disorders that affect the frontal lobes can cause
1. detrusor hyperactivity
2. or altered social behavior regarding micturition

no inhibition on pontine micturition center when bladder is filled

294
Q

Disturbance of Defecation

A
  • Fecal retension - caused by transverse lesion of Spinal cord above L1-2 (where hypogastric nerve originates)
  • fecal incontinence: lesion of sacral segments
295
Q

most vulnerabel spots for spinal cord injury

A

border between rigid and flexible regions (
1. craniocervical, CC
2. cervicothoracal, CT
3. thoracolumbar zones

296
Q

types of spinal cord injury

A

Acute transverse
Brown-Sequard syndrom
Anterior cord
Central cord
Conus medullaris
Spinal cord concussion
Cauda equina syndrom

297
Q

Genetic background of alzheimers disease

A

AD
genetic risk factor: ApoE epsilon4 allele ( 1 increases risk by 2-3, 2 alleles increase risk by 10x)
* monogenic form:
*beta-amyloid precursor protein (APP)
*Presenilin-1 mutation
*Presenilin-2 mutation

  • Polygenic: multiple genes, and environmental
298
Q

Genetic bckground of frontotemporal dementia

A
  • Polygenic, complex inheritance
  • Autosomal Dominant (AD) in 20-50% of cases
  • mutations of 2 genes:
    *Microtubule ass. protein tau gene MAPT -> tau protein
    *GRN encodes progranulin

due to mutations pathologic proteins are expressed which aggregate in neurons

299
Q

Huntington’s disease definition

A

Neurodegenerative disorder causing progressive, selective (localized) neural cell death
associated with choreic movement and dementia

300
Q

what is huntington disease associated with

A

associated with
* choreic movement
* dementia

301
Q

Etiology of Huntingtons disease

A

increased length of a CAG tripplet repeat present in the huntington gene on chr 4p16.3

CAG repeats is normally < 36 (average 19)
in pts with mutated HD gene the repeat size is between 36-121
the higher the no. the worse the course with earlier onset, more severe, quicker progression

302
Q

prevelance of HD

A

4-8/100,000
no difference in gender

303
Q

when do symptoms start in HD

A

between 3rd-5th decade
lasting on average 10-15 years

10% had juvenile onset
20% late onset mild HD

more severe with earlier onset in each succeeding generation (anticipation)

304
Q

cause of death in HD

A

deterioration of somatic condition
associated with secondary diseases

305
Q

pathomechanism of HD-which areas affected in nervous system?

A

most prominent changes in
* caudate
* putamen
* substantial nigra
* cerebral cortex
* hippocampus
* purkinje cells in cerebellum

306
Q

which neurons are most vulnerable in HD

A

striatal spiny neurons

307
Q

what does CAG code for

A

glutamine -> polyglutamine tract
> production of altered 3D forms of protein that aggregates, forms neuronal inclusion bodies, toxic protein fragments > metabolic stress > altered DNA expression and protein-protein interaction

308
Q

signs and symptoms of HD

A
  • Motor symptoms: chorea, hyperkinesia, rigidity, dysarthia
  • Psychopathological: irritation, impulsivity, aggression, depression
  • cognitive decline, dementia:
    *memory loss, slow data processing
    *already present from the beginning
309
Q

first motor sign in HD

A

often CN3 occulomotor function disturbance
then orofacial dyskinesia (continuous grinning)

later dyskinesia appears in other muscle groups (generalized chorea)

even later stages: bradykinesia, rigidity, dystonia may dominate

310
Q

what is chorea

A

brief, quasipurposeful, irregular muslce contractions that are not repetitive or rhythmic
but flow from one muscle group to the next

311
Q

diagnosis of HD

A
  • clinical sign
  • postive family history
  • genetic testing (if negative, do MRI to rule out inflammatory, autoimmune or neurodegenrative CNS disorders)
312
Q

TX of HD

A

symptomatic
* SSRI, mirtazapine, sulpiride for depression
* neuroleptic drugs : clozapine, olanzapine, tiapride, tetrabenazine, amantidine) for hyperkinesia

313
Q

fragile X definition

A

x-linked dominant disorder
causes range of developmental problems :
* learning disability
* cognitive impairment
males more severely affected

314
Q

fragile x ETIOLOGY

A

> 200 CGG repeats in FMR1 (Fragile x messenger ribonucleoprotein 1) (normally 5-40 repeats
causes FMRP protein defiency (regulates production of other proteins and plays roles in development of synapses)
distruption of nervous system functions

premutation (55-200 repeats) milder version of disease

315
Q

fragile x signs and symptoms

A

delayed development of speech and language by age 2
intelectual disability (mild/moderate)
children may have anxiety, hyperactive behaviour, attention deficit disorder or autism
seizures
characteristic physical features:
* long
* narrow face, large ears
* prominent jaw, forehead
* flexible fingers
* flat feet
* enlarged testicles after puberty

316
Q

fragile x diagnosis

A

molecular testing

317
Q

fragile x tx

A

speech and language therapy
special education in children

neuro (32 decks)

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