Neurologic emergencies Flashcards
Cheyne-stokes breathing
Periods of hyperpnoea followed by brief periods of apnoea
Diffuse cerebral or thalmic disease and metabolic encephalopathies
Central neurogenic hyperventilation
Persistant hyperventilation that can induce respiratory alkalosis
Midbrain lesions
Apneusis
Pauses in breathing at full inspiration
Pontine lesions
Irregular/ataxic breathing
Irregular frequency & depth of respiration before complete apnoea
Lower pons & medulla
Unilateral mydriatic, unresponsive pupil
Loss of parasympathetic innervation to the eye indicating destruction or compression of ipsilateral midbrain for CNIII.
Increased ICP, cerebral herniation
Bilateral miosis
Metabolic encephalopathies, diffuse midbrain compression with increased ICP
Bilateral, mydriatic, unresponsive pupils
Severe, bilateral compression or destruction of midbrain or CNIII
Bilateral cerebral herniation
Grave prognosis
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
B
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
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
Which nerve fibers are responsible for sensing temperature:
a. Autonomic afferent
b. Somatic afferent
c. Autonomic efferent
d. Somatic efferent
B
A patient that responds only to noxious stimulation is:
a. comatose
b. stuporous
c. obtunded
d. lethargic
B
A clinical factor that can increase intracranial pressure is:
a. decreased PaCO2
b. hypothermia
c. increased PaO2
d. coughing
D
Cerebral blood flow is equal to which of the following?
a. CPP/CVR
b. CVR/CPP
c. MAP–ICP
d. ICP–MAP
A
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
Which toxin should be considered if a patient presents for tremor/seizure activity?
a. Ibuprofen
b. Grapes
c. Metaldehyde
d. Garlic
C
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
B
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
B
Serotonin
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
Obtund
Decreased response to external stimuli
Stupor
Response only to noxious stimuli
Coma
No conscious response to stimuli.
+- cranial nerve reflexes
Cerebrum
Integrates information and planning of motor activity, specific response to information input and responsible for emotion & memory
Reticular activating system
Activates the cerebral cortex and maintains consciousness
Seizures indicate
Cerebral cortisol dysfunction and may be due to an extracranial or intracranial process.
Decerebrate activity
Opisthotonos and extensor rigidity of all four limbs; associated with stupor or coma. Indicates lesion of rostral pons and midbrain.
Decerebellate rigidity
Associated with acute cerebellar lesions. Opisthotonus and extensor of thoracic limbs and +- hind limbs; patient generally responsive.
Basic neurological evaluation
- LOC
- Motor activity
- Pupil size & reactivity
- Respiratory patterns
- Oculocephalic reflexes
- form basis for coma scales
Pupil size
Balance between sympathetic and parasympathetic innervation. Loss of parasympathetic innervation indicates deteriorating patient status and is identified by unilateral or bilateral mydriasis
Causes of pupil size changes
1 structural lesions
Other: metabolic and some drugs
Loss of oculocephalic reflexes
Generally associated with lesions of medial longitudinal fasciculus (pons & midbrain) which normally coordinates CN 3, 4, 6 and usually indicates poor prognosis.
Increase in ICP
CSF and blood compartment must reduce to compensate > reduced cerebral blood flow to prevent further increases in ICP
MGCS
Facilitates assessment of prognosis
Assesses motor function, LOC and brainstem reflexes and scores /18 (18 normal)
Doesn’t predict long-term functional outcome
Initially miotic pupils that become mydriatic
Indicate progressive brainstem lesion
PLR
Assess the optic nerve function
Changes can be unilateral or bilateral
Fixed dilated pupils (mydriasis)
May indicate irreversible midbrain lesion or advanced herniation
Miosis
May still indicate adequate function of rostral brainstem, optic chiasm, optic nerve and retina
Seizures
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.
Types of epilepsy
Idiopathic
Symptomatic
Cryptogenic
What is termed cluster seizures
2 or more seizures within a 24h period
Status epilepticus
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.
Minimum database for seizure disorders
CBC
Biochemistry
24h fasted glucose
Bile acids
Urinalysis
+- Advanced imaging (EEG, MRI, CT)
Benzodiazepines for seizures
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
Barbiturates for seizure disorders
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
Refractory seizures
Propofol and light anaesthesia/deep sedation
Propofol is a GABA agonist
Long term anticonvulsant therapy
Phenobarbital + bromide +- levetiracetam
Spinal cord ischaemia
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.
Neurological scoring
Grade 1 = no deficits
Grade 2 = paresis, walking
Grade 3 = paresis, non-ambulatory
Grade 4 = paralysis
Grade 5 = paralysis, no deep pain
UMN signs
In the CNS (brain, spinal cord)
- hyperreflexia
- increased muscle tone/spasticity
- spastic paralysis
LMN signs
Anterior horn to the muscle
- atrophy
- paresis/paralysis
- hyporeflexia
- decreased muscle tone
- flaccidity
S1 to S3 spinal lesion
LMN signs
Sciatic, pudendal, perineal nerves involved
Flaccidity, decreased segmental reflexes
Urinary and faecal incontinence
Pelvic limb paresis without completely absent withdrawal
L4 to S1 spinal lesion
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
T3 to L3 spinal lesion
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
C6 to T2 spinal lesion
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
C1 to C5 spinal lesion
UMN in all limbs and respiration may be shallow or absent due to loss of phrenic and intercostal nerve function
Treatment for spinal cord injury
- IVFT to support spinal cord vasculature and optimise arterial blood flow
- Stabilise F# and keep patient immobile where indicated
- Refer to surgeon and have surgery performed if indicated
- General supportive care measures I.e. pain relief, antispasmodics, nutrition, comfort, wounds etc
ICH
Intracranial hypertension
When the ICP increases above its range of 5-12mmHg resulting in neurological abnormalities
CSF
Ultrafiltration of fluid from the blood volume of choroid plexus
BBB
Tightly regulates solutes entering the brain but is permeable to water
Cerebral perfusion pressure
CPP = MAP - ICP
An increase in cerebral blood flow due to dilation
Increases cerebral blood volume leading to increased ICP
A decrease in cerebral blood flow due to constriction
Leads to decreased cerebral blood volume and reduced ICP
3 homeostatic mechanisms to maintain normal ICP
- Volume buffering; intracranial volume fixed so increases in one compartment means a compensatory fall in others
- Autoregulation; arteriole resistance changes and operates between 50-150mmHg
- Cushing response; bradycardia and severe hypertension, as well as mentation abnormalities
Neurological exam
- LOC
- Brainstem reflexes
- Motor function
- Respiration
Treatment of ICH
HTS/Mannitol
Furosemide
Head elevation 30 degrees
Avoid jugular compression
Oxygen therapy
IVFT
Prevent hypotension & hypoxia
Manage neurological and inflammatory signs
Other supportive therapies
Mannitol
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
HTS 7%
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
Minimum database for patients suspected to motor unit disease
CBC & Biochemistry
T4
Cortisol/ACTH stim
Glucose
Urinalysis, C&S
CK
Tox screening
Advanced imaging
Neurapraxia
Loss of nerve conduction without structural changes (transient loss of blood supply)
Axonotmesis
Axonal damage without loss of supporting structures (axonal regeneration required)
Neurotmesis
Complete severance of a nerve
Tetanus
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).
Tetanus signs
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)
Treatment of tetanus
Neutralise unbound toxin (100-1000U/kg max 20000U)
Remove source of infection
Control rigidity & spasms
Aggressive supportive care I.e. nutrition, comfort etc
Dysfunction to vestibular system
Disequilibrium and clinical signs usually point to side of brain affected
Horners
- Miosis
- Enopthalmos
- Ptosis
- Protrusion of the third eyelid
HE
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
Treatment of HE
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
Diagnosis of HE
Bile acids
Ammonia
Liver function test
Imaging
Traumatic brain injury pathophysiology
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
Systemic and intracranial injuries that perpetuate TBI
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
Cerebral blood flow
Ability to maintain constant between MAP 50-150mmHg
CBV = CPP and CR
This is impaired in TBI so ischaemia more likely
- CPP = MAP -ICP
Monro-kellie doctrine
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
Considerations for TBI patients
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
Treatment for TBI
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
Which cranial nerve helps control eye movement?
a. CN I
b. CN III
c. CN V
d. CN VIII
B
What is the correct term for dilation of the pupils?
a. Anisocoria
b. Blepharospasm
c. Miosis
d. Mydriasis
D
Which disease does not typically result in anterior uveitis?
a. Panleukopenia
b. FeLV
c. FIV
d. Toxoplasmosis
A
Hyphema refers to the collection of blood in which area of the eye?
a. Cornea
b. Anterior chamber
c. Posterior chamber
d. Sclera
B
What is a full-thickness defect of the cornea called?
a. Descemetocele
b. Corneal abrasion
c. Corneal ulcer
d. Proptosis
A
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
C
Retinal detachment is often a sequela of what process?
a. Increased IOP
b. Respiratory distress
c. Distemper
d. Systemic hypertension
D
Anterior flare may be present in a patient suffering from which condition?
a. Proptosis
b. Uveitis
c. Anisocoria
d. Corneal ulceration
B
The pigmented portion of the eye that surrounds the pupil is which structure?
a. Lens
b. Ciliary body
c. Iris
d. Retina
C
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
B
Normal ICP
5-12mmHg
