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VTS(ECC) Preparation > Neurologic emergencies > Flashcards

Neurologic emergencies Flashcards

1
Q

Cheyne-stokes breathing

A

Periods of hyperpnoea followed by brief periods of apnoea

Diffuse cerebral or thalmic disease and metabolic encephalopathies

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2
Q

Central neurogenic hyperventilation

A

Persistant hyperventilation that can induce respiratory alkalosis

Midbrain lesions

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3
Q

Apneusis

A

Pauses in breathing at full inspiration

Pontine lesions

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4
Q

Irregular/ataxic breathing

A

Irregular frequency & depth of respiration before complete apnoea

Lower pons & medulla

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5
Q

Unilateral mydriatic, unresponsive pupil

A

Loss of parasympathetic innervation to the eye indicating destruction or compression of ipsilateral midbrain for CNIII.

Increased ICP, cerebral herniation

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6
Q

Bilateral miosis

A

Metabolic encephalopathies, diffuse midbrain compression with increased ICP

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7
Q

Bilateral, mydriatic, unresponsive pupils

A

Severe, bilateral compression or destruction of midbrain or CNIII

Bilateral cerebral herniation
Grave prognosis

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8
Q

In patients with traumatic brain injury, it is important to maintain a normal MAP and to closely monitor the patient’s:
a. electrocardiogram
b. ventilation
c. range of motion
d. potassium

A

B

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9
Q

Which of the following can occur after blood flow is suddenly restored after using a clot dissolution drug?
a. Hyperkalemia
b. Azotemia
c. Hypotension
d. Respiratory alkalosis

A

A

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10
Q

Patients suffering from upper motor neuron injury can also suffer dysfunction of:
a. the urinary bladder
b. the gastrointestinal system
c. the cardiac system
d. the brain

A

A

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11
Q

Which nerve fibers are responsible for sensing temperature:
a. Autonomic afferent
b. Somatic afferent
c. Autonomic efferent
d. Somatic efferent

A

B

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12
Q

A patient that responds only to noxious stimulation is:
a. comatose
b. stuporous
c. obtunded
d. lethargic

A

B

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13
Q

A clinical factor that can increase intracranial pressure is:
a. decreased PaCO2
b. hypothermia
c. increased PaO2
d. coughing

A

D

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14
Q

Cerebral blood flow is equal to which of the following?
a. CPP/CVR
b. CVR/CPP
c. MAP–ICP
d. ICP–MAP

A

A

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15
Q

Cushing’s reflex is defined as:
a. hypertension and bradycardia
b. hypotension and tachycardia
c. absent PLR and decreased level of consciousness
d. present PLR and decreased level of consciousness

A

A

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16
Q

Which toxin should be considered if a patient presents for tremor/seizure activity?
a. Ibuprofen
b. Grapes
c. Metaldehyde
d. Garlic

A

C

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17
Q

Which drug class is considered the first line of treatment in non-hypoglycemic seizures?
a. NMDA antagonists
b. Benzodiazepines
c. Phenothiazines
d. Alpha-2 agonists

A

B

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18
Q

Which drug class is considered the first line of treatment in non-hypoglycemic seizures?
a. NMDA antagonists
b. Benzodiazepines
c. Phenothiazines
d. Alpha-2 agonists

A

B

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19
Q

Serotonin

A

Serotonin actions (enterochromaffin): platelet aggregation, vasoconstriction, uterine contraction, peristalsis and bronchoconstriction. Either excreted by lungs or transported to platelets
Central serotonin: influences mood, aggression, sleep, thermoregulatiom, vomiting and pain perception.

Serotonin is formed by AA tryptophan, synthesised and stored in enterochromaffin cells and myenteric plexus in the GI tract

Synthesised in neuronal cytosol, stored in vesicles at nerve terminals and released into the synaptic cleft where it binds to post-synaptic receptor mediating transmission. It is inactivated by MAOI to form 5-HT and then eliminated by urine

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20
Q

Obtund

A

Decreased response to external stimuli

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21
Q

Stupor

A

Response only to noxious stimuli

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22
Q

Coma

A

No conscious response to stimuli.
+- cranial nerve reflexes

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23
Q

Cerebrum

A

Integrates information and planning of motor activity, specific response to information input and responsible for emotion & memory

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24
Q

Reticular activating system

A

Activates the cerebral cortex and maintains consciousness

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25
Q

Seizures indicate

A

Cerebral cortisol dysfunction and may be due to an extracranial or intracranial process.

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26
Q

Decerebrate activity

A

Opisthotonos and extensor rigidity of all four limbs; associated with stupor or coma. Indicates lesion of rostral pons and midbrain.

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27
Q

Decerebellate rigidity

A

Associated with acute cerebellar lesions. Opisthotonus and extensor of thoracic limbs and +- hind limbs; patient generally responsive.

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28
Q

Basic neurological evaluation

A
  1. LOC
  2. Motor activity
  3. Pupil size & reactivity
  4. Respiratory patterns
  5. Oculocephalic reflexes
  • form basis for coma scales
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29
Q

Pupil size

A

Balance between sympathetic and parasympathetic innervation. Loss of parasympathetic innervation indicates deteriorating patient status and is identified by unilateral or bilateral mydriasis

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30
Q

Causes of pupil size changes

A

1 structural lesions

Other: metabolic and some drugs

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31
Q

Loss of oculocephalic reflexes

A

Generally associated with lesions of medial longitudinal fasciculus (pons & midbrain) which normally coordinates CN 3, 4, 6 and usually indicates poor prognosis.

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32
Q

Increase in ICP

A

CSF and blood compartment must reduce to compensate > reduced cerebral blood flow to prevent further increases in ICP

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33
Q

MGCS

A

Facilitates assessment of prognosis
Assesses motor function, LOC and brainstem reflexes and scores /18 (18 normal)
Doesn’t predict long-term functional outcome

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34
Q

Initially miotic pupils that become mydriatic

A

Indicate progressive brainstem lesion

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35
Q

PLR

A

Assess the optic nerve function
Changes can be unilateral or bilateral

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36
Q

Fixed dilated pupils (mydriasis)

A

May indicate irreversible midbrain lesion or advanced herniation

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37
Q

Miosis

A

May still indicate adequate function of rostral brainstem, optic chiasm, optic nerve and retina

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38
Q

Seizures

A

Clinical manifestation of paroxysmal cerebral disorder cause by synchronous, excessive electrical neuronal discharge which comes from the cerebral cortex. They may be partial/localised or complex/generalised.

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39
Q

Types of epilepsy

A

Idiopathic
Symptomatic
Cryptogenic

40
Q

What is termed cluster seizures

A

2 or more seizures within a 24h period

41
Q

Status epilepticus

A

Abnormal brain homeostasis mechanisms that usually prevent seizures. Can be due to neuronal excitation, inadequate neuronal inhibition and excess neurotransmitters leading to ATP depletion and build up of lactate ultimately leading to neuronal necrosis.

42
Q

Minimum database for seizure disorders

A

CBC
Biochemistry
24h fasted glucose
Bile acids
Urinalysis
+- Advanced imaging (EEG, MRI, CT)

43
Q

Benzodiazepines for seizures

A

Diazepam or midazolam; 0.5-1mg/kg and 0.2mg/kg respectively
Bind to GABA receptors and hyperpolarise neurons to decrease neuronal firing.
Diazepam fat soluble whereas midazolam water soluble

44
Q

Barbiturates for seizure disorders

A

Provided if SE non-responsive to benzodiazepines or for control of long term seizure disorders
Phenobarbital and levetiracteam most common
Pheno may cause sedation, respiratory depression, hypotension and death

45
Q

Refractory seizures

A

Propofol and light anaesthesia/deep sedation
Propofol is a GABA agonist

46
Q

Long term anticonvulsant therapy

A

Phenobarbital + bromide +- levetiracetam

47
Q

Spinal cord ischaemia

A

Decreased blood flow and/or loss of autoregulation, vasospasm and haemorrhage > ischaemia… cytosine oedema, axonal degeneration, demyelination, abnormal impulse transmission, conduction block and cellular death.

48
Q

Neurological scoring

A

Grade 1 = no deficits
Grade 2 = paresis, walking
Grade 3 = paresis, non-ambulatory
Grade 4 = paralysis
Grade 5 = paralysis, no deep pain

49
Q

UMN signs

A

In the CNS (brain, spinal cord)
- hyperreflexia
- increased muscle tone/spasticity
- spastic paralysis

50
Q

LMN signs

A

Anterior horn to the muscle
- atrophy
- paresis/paralysis
- hyporeflexia
- decreased muscle tone
- flaccidity

51
Q

S1 to S3 spinal lesion

A

LMN signs
Sciatic, pudendal, perineal nerves involved
Flaccidity, decreased segmental reflexes
Urinary and faecal incontinence
Pelvic limb paresis without completely absent withdrawal

52
Q

L4 to S1 spinal lesion

A

Femoral, sciatic, pupendal, obturator & pelvic nerves involved
Pelvic limb, tail & anus dysfunction. Normal thoracic function.
Short-strided gait and shuffling paws
Plato grade or weak stance
Diminished or absent pelvic reactions

53
Q

T3 to L3 spinal lesion

A

UMN signs caudal to the lesion
Paresis/paralysis/spasticity
Exaggerated reflexes, cross-extensor
Limited to the pelvic limbs
Urinary retention and faecal incontinence
Abnormal cutaneous trunchi reflex approx. L3
Schiff-Sherrington phenomenon

54
Q

C6 to T2 spinal lesion

A

UMN signs to the pelvic limbs and LMN to the thoracic limbs
Subscapular, suprascapula, musculocutaneous, axillary, radial, median and ulna nerves
Neuropathic lameness
Absent cutaneous trunchi reflex
Decreased thoracic movement

55
Q

C1 to C5 spinal lesion

A

UMN in all limbs and respiration may be shallow or absent due to loss of phrenic and intercostal nerve function

56
Q

Treatment for spinal cord injury

A
  1. IVFT to support spinal cord vasculature and optimise arterial blood flow
  2. Stabilise F# and keep patient immobile where indicated
  3. Refer to surgeon and have surgery performed if indicated
  4. General supportive care measures I.e. pain relief, antispasmodics, nutrition, comfort, wounds etc
57
Q

ICH

A

Intracranial hypertension
When the ICP increases above its range of 5-12mmHg resulting in neurological abnormalities

58
Q

CSF

A

Ultrafiltration of fluid from the blood volume of choroid plexus

59
Q

BBB

A

Tightly regulates solutes entering the brain but is permeable to water

60
Q

Cerebral perfusion pressure

A

CPP = MAP - ICP

61
Q

An increase in cerebral blood flow due to dilation

A

Increases cerebral blood volume leading to increased ICP

62
Q

A decrease in cerebral blood flow due to constriction

A

Leads to decreased cerebral blood volume and reduced ICP

63
Q

3 homeostatic mechanisms to maintain normal ICP

A
  1. Volume buffering; intracranial volume fixed so increases in one compartment means a compensatory fall in others
  2. Autoregulation; arteriole resistance changes and operates between 50-150mmHg
  3. Cushing response; bradycardia and severe hypertension, as well as mentation abnormalities
64
Q

Neurological exam

A
  1. LOC
  2. Brainstem reflexes
  3. Motor function
  4. Respiration
65
Q

Treatment of ICH

A

HTS/Mannitol
Furosemide
Head elevation 30 degrees
Avoid jugular compression
Oxygen therapy
IVFT
Prevent hypotension & hypoxia
Manage neurological and inflammatory signs
Other supportive therapies

66
Q

Mannitol

A

Immediately induces plasma volume expansion and increases CBF resulting in better delivery of oxygen to the brain due to osmotic shifts (takes 15-30 min).
Recommended 0.5-1g/kg of 20% over 20min and lasts 1-3 hours

67
Q

HTS 7%

A

Similar effects as mannitol but less likely to induce hypotension and also has benefits on the excitatory neurotransmitters and the immune system

4ml/kg over 10min

68
Q

Minimum database for patients suspected to motor unit disease

A

CBC & Biochemistry
T4
Cortisol/ACTH stim
Glucose
Urinalysis, C&S
CK
Tox screening
Advanced imaging

69
Q

Neurapraxia

A

Loss of nerve conduction without structural changes (transient loss of blood supply)

70
Q

Axonotmesis

A

Axonal damage without loss of supporting structures (axonal regeneration required)

71
Q

Neurotmesis

A

Complete severance of a nerve

72
Q

Tetanus

A

Caused by bacterium clostridium tetani (G+ anaerobe, spore-forming, motile, non-encapsulated) that releases neurotoxins tetanospasm & tetanolysin during its vegetative stage which inhibits motor neurons, affects inhibitory control (GABA) and dyregulates autonomacity. Neuronal binding leads to sympathetic over-reactivity and once bound to neurons cannot be reversed and new terminals must be created (prolonged recovery).

73
Q

Tetanus signs

A

Sardonic grin
Localised signs proximal to entry site
Muscle rigidity and spasms, increased muscle tone
Trismus
Dyspnoea
Stiff gait
Opisthotonus
Seizures
Respiratory paralysis
Dysphagia
Autonomic dysregulation (HR, BP, temp)

74
Q

Treatment of tetanus

A

Neutralise unbound toxin (100-1000U/kg max 20000U)
Remove source of infection
Control rigidity & spasms
Aggressive supportive care I.e. nutrition, comfort etc

75
Q

Dysfunction to vestibular system

A

Disequilibrium and clinical signs usually point to side of brain affected

76
Q

Horners

A
  1. Miosis
  2. Enopthalmos
  3. Ptosis
  4. Protrusion of the third eyelid
77
Q

HE

A

Hepatic encephalopathy
Accumulation of ammonia in systemic circulation due to severe liver insufficiency such as PSS. The accumulation of ammonia passes the BBB decreasing excitory neuro transmission by downregulatimg NMDA receptors and chloride extrusion from post-synaptic neurons. Induces seizures and neurotoxicity

78
Q

Treatment of HE

A

IVFT
Attenuation of PSS if present
Reduce ICP
Seizure control
Colloids
Glucose
Electrolyte supplementation
Broad spectrum AB
Lactulose/enemas
Low protein (14-17%) diet that is high in carbs
GI protectants

79
Q

Diagnosis of HE

A

Bile acids
Ammonia
Liver function test
Imaging

80
Q

Traumatic brain injury pathophysiology

A

Primary injury +- results in displacement of the brain within the skull (concussion less severe, laceration most severe) leading to haemorrhage and oedema > secondary injury involves a cascade of biochemical events including massive catecholamine/neuroexcitory release, N.O production, compression of the brain > there is influx of Na, Cl and Ca into brain cells, free radical release, influx of inflammatory mediators > disruption of the BBB occurs and there is increased ICP as well as ATP depletion (vasodilation and inflammatory response), activation of coagulation > neuronal death as CPP worsens and cycle continues

81
Q

Systemic and intracranial injuries that perpetuate TBI

A

Systemic: hypoxaemia, hypo- or hyper- capnoea, hypo- or hyper- thermia, hyper- or hypo- tension, hypo- or hyper- glycaemia, SIRS
Intracranial: increased ICP, compromised BBB, oedema, mass lesions, vasospasm, seizures, infection

82
Q

Cerebral blood flow

A

Ability to maintain constant between MAP 50-150mmHg
CBV = CPP and CR
This is impaired in TBI so ischaemia more likely

  • CPP = MAP -ICP
83
Q

Monro-kellie doctrine

A

V intracranial - V brain + V CSF + V blood + V mass lesion
Increases in one area increase ICP and try to counter regulate that increase by decreasing
There is a fixed amount of volume in the brain so increases can be a risk factor for poor CBF and herniation

84
Q

Considerations for TBI patients

A

Avoid jugular compression
Watch and treat cushings reflex
Elevate head 15-30 degrees
Maintain CO2 25-35mmHg
Prevent hypoxaemia and hypotension
0.9% NaCl fluid of choice because of the least amount of free water
Mydriasis +- strabismus associated with grave to poor outcome
Avoid furosemide to avoid IV depletion

85
Q

Treatment for TBI

A

Mannitol: reduces ICP, improves CBF, free radical scavenging, decreases blood viscosity, lasts 1.5-6h (blouses > CRI)
HTS: reduces ICP, improves CBF, less risk of hypotension compared to mannitol, vasoregulates, immunomodulatory, improves haemodynamic status
Oxygen +- ventilation
Head elevation
+- therapeutic hypothermia
+- anti seizure meds
Fluid resuscitation to maintain MAP 80-100mmHg

86
Q

Which cranial nerve helps control eye movement?
a. CN I
b. CN III
c. CN V
d. CN VIII

A

B

87
Q

What is the correct term for dilation of the pupils?
a. Anisocoria
b. Blepharospasm
c. Miosis
d. Mydriasis

A

D

88
Q

Which disease does not typically result in anterior uveitis?
a. Panleukopenia
b. FeLV
c. FIV
d. Toxoplasmosis

A

A

89
Q

Hyphema refers to the collection of blood in which area of the eye?
a. Cornea
b. Anterior chamber
c. Posterior chamber
d. Sclera

A

B

90
Q

What is a full-thickness defect of the cornea called?
a. Descemetocele
b. Corneal abrasion
c. Corneal ulcer
d. Proptosis

A

A

91
Q

An IOP reading of greater than 25^mmHg suggests what disease process?
a. Anterior uveitis
b. Lens luxation
c. Acute glaucoma
d. Progressive retinal atrophy

A

C

92
Q

Retinal detachment is often a sequela of what process?
a. Increased IOP
b. Respiratory distress
c. Distemper
d. Systemic hypertension

A

D

93
Q

Anterior flare may be present in a patient suffering from which condition?
a. Proptosis
b. Uveitis
c. Anisocoria
d. Corneal ulceration

A

B

94
Q

The pigmented portion of the eye that surrounds the pupil is which structure?
a. Lens
b. Ciliary body
c. Iris
d. Retina

A

C

95
Q

Which cranial nerve is responsible for sending images to the brain for processing?
a. CN I
b. CN II
c. CN VI
d. CN X

A

B

96
Q

Normal ICP

A

5-12mmHg

VTS(ECC) Preparation (21 decks)

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