Neurology Flashcards
What are the two main neurotransmitter in autonomic nerve system and what are the fibers they are secreted from?
Acetylcholine - cholinergic nerve fiber
Norepinephrine - adrenergic nerve fiber
Component of complete neurological exam
- mentation
- gait
- cranial nerve
- segmental reflexes
- proprioception
- palpation
- nociception
Paresis vs plegia
Paresis = weakness
Plegia = paralysis
True or False:
In the autonomic nerve system, all the pre-ganglionic neurons are cholinergic, no matter they belong to sympathetic or parasympathetic.
True
What are the differences between muscarinic and nicotinic receptors?
Muscarinic:
- G protein receptors
- Locates at all the effector cells at the end of all the parasympathetic nerve ending and some sympathetic nerve ending (e.g. sweat gland)
Nicotinic:
- Ligand-gated ion channels
- Locates at the autonomic nerve system synapses between preganglion and postganglion, somatic nerve ending (skeletal muscles)
Is SNS or PNS also called craniosacral division of ANS?
PNS
- SNS is also called thoracolumbar division of the autonomic nerve system
Parasympathetic nerve fibers leave the CNS through which cranial nerves and which nerve in the sacral region?
3, 7, 9, 10 (75%)
Pelvic nerves
What is the resting membrane potential for neuron?
-70 mV
Which part of the brain do thalamus and hypothalamus belong to?
Forebrain
Where is medulla oblongata?
Brainstem (connecting the brainstem to the spinal cord)
Where are the grey matter and white matter in the brain and spinal cord?
Brain: grey matter outside, white matter inside
Spinal cord: grey matter inside, white matter outside
Which spinal nerve root carries afferent neurons and which one carries efferent neurons?
Dorsal: afferent neurons
Ventral: efferent neurons
On MRI T1-weighing, what tissue is hyperintense and what tissue is hypointense? What about T2-weighing and fluid attenuated inversion recovery (FLAIR)?
T1:
- Fat hyperintense
- Fluid (e.g. CSF) hypointense
T2:
- Fluid and tissue with high fluid content hyperintense
- Fat variable
* also called “pathology scan” → inflammation, bleeding, edema will be whither
FLAIR
- Pure fluid (e.g. CSF, cystic fluid) become hypointense → facilitate differentiating
What is the difference between acute brain hemorrhage and chronic brain hemorrhage on the MRI T1 and T2 window?
T1
- Acute (< 24 hours): isointense or hypointense
- Chronic: hypointense
T2
- Acute: hyperintense
- Chronic: hypointense
Describe decerebrate rigidity and the lesion localization.
Stupuros/comatosen + opisthotonus and extension of all limbs
Lesion: rostral pons and midbrain
Describe decerebellate rigidity and the lesion localization.
Normal mentation + opisthotonus with extensor rigidity of the thoracic limbs and either extension or flexion of the pelvic limbs is present
Lesion: cerebellum
Describe Cheyne-Stokes breathing.
Periods of hyperpnea alternating with periods of apnea; can be seen with diffuse cerebral or thalamic disease and metabolic encephalopathies
Describe central neurogenic hyperventilation and the lesion.
Persistent hyperventilation that may result in respiratory alkalosis
Midbrain lesions
When a patient has decrease or absent PLR, where is the lesions?
Midbrain, CN II & III (PNS)
When a patient loses its oculocephalic reflex, where is the lesion?
CN 3, 6, 8
How will the left eye CN II injury affect the PLR?
When light shines to the left eye, there will be no PLR in both eye; when the light shines to the right eye, there will be direct and consensual PLR in both eyes
How will the left eye CN III injury affect the PLR?
When the light shines to the left eye, there will be consensual PLR to the right eye but no PLR in the left; when the light shines to the right eye, there will be direct PLR at the right eye but no consensual PLR to the left eye.
When the patient is miotic and there is no ocular injury, where is the lesion?
diencephalon (e.g. thalamus, hypothalamus)
- Hypothalamus is the origin of SNS pathway
What are the three categories of seizures?
1) Reactive
2) Structural
3) Idiopathic
What is MOA for phenobarbital?
Bind to GABAa receptor and enhance its activity (between beta and gamma subunits)
AMPA antagonist
Ca++ channel inhibitor
How do you load phenobarbital?
4 mg/kg IV q6h for 4 doses, and then switch to 2.5 mg/kg PO q12h
What are the 4 nerves that come from the S1-S3?
Sciatic, pelvic, pudendal, perineal nerves
What are the 5 nerves that come from the L4-S1?
Femoral, pelvic, sciatic, pudendal, obturator nerves
Describe Schiff-Sherrington phenomenon and the pathophysiology.
- Thoracic limb extension and inability to move the pelvic limbs normally. Normal CP at thoracic limbs. Normal spinal reflex at pelvic limbs.
- Indicates T-L spinal cord injury
- Pathophysiology: a lack of ascending inhibitory input to the thoracic limbs originating from the border cells located in the lower thoracic and lumbar spinal cord
- Border cells are responsible for tonic inhibition of extensor muscle α-motor neurons in the cervical intumescence.
When you see two-engine gaits, it most likely indicates which part of the spinal cord injury?
C6 - T2
Thoracic limb: short-stride gait
Pelvic limb: spinal ataxia
Define spinal shock.
Profound depression of segmental reflexes caudal to a lesion, despite reflex arcs remaining physically intact
- It can be up to 12-24 hours after injury
True or False: The spinal cord extends more caudally in cats compared to dogs.
True
When a patient has ventrolateral strabismus, it indicates which CN dysfunction?
CN III
True or False: Trigeminal nerve has both sensory and motor function.
True
What are the three branches of trigeminal nerve and which one has both sensory and motor function?
Ophthalmic (sensory only)
Maxillary (sensory only)
Mandibular (both motor and sensory)
What does the palpebral reflex test for?
Sensory - trigeminal nerve (CN 5)
Medial canthus (ophthalmic branch)
Lateral canthus (maxillary branch)
Motor - facial nerve (CN 7)
What does menace response test for?
CN 2, 7
Which CN is responsible for tear production?
CN 7
What does the pelvic limb withdrawal reflex test for?
L6-S1 and sciatic nerve
What does the patellar reflex test for?
L4-L6 and femoral nerve
What does the gastrocnemius reflex test for?
L7-S1 and tibial nerve
Why KBr is not recommended in cats?
Can cause pneumonitis
What is the recommended serum phenobarbital level in dogs? When should you pull the blood after drug administration?
15-35 mcg/dL (higher than 35 mcg/dL is usually associated with liver injury)
6-8 hours after drug administration
What is normal serum KBr level in dogs?
When KBr is used alone: 0.8 - 3 mg/ml
When combined with phenobarbital: 0.8 - 2.4 mg/ml
True or False: For vestibular ataxia, the side of the head tilt usually indicates the side of the lesion.
True
What is the normal range of intracranial pressure?
5-12 mmHg
What is the formula for cerebral perfusion pressure?
CPP = MAP - ICP
What are the three mechanisms to maintain ICP?
1) Cushing reflex
2) Autoregulation
3) Volume buffering
Explain Monro-Kellie doctrine.
The sum of volumes of brain, CSF, and intracranial blood is constant. An increase in one should cause a decrease in one or both of the remaining two
Explain how the brain autoregulates the cerebral blood flow.
1) Pressure autoregulation
- When the CPP is within the range of 50-150 mmHg, the brain is able to maintain the stable cerebral blood flow via vascular myogenic reflex
2) Chemical autoregulation
- High PaCO2, low PaO2, high H+ → vasodilation
Explain the pathophysiology of Cushing reflex.
Decompensated intracranial hypertension → decreased cerebral blood flow and increased CO2 → catecholamine release → systemic vasoconstriction → activates baroreceptors → bradycardia
What is the ideal CPP in dogs and cats?
50 - 90 mmHg
What are the 2 effects of mannitol in treating ICH?
1) Immediate volume expansion effect → improves cerebral blood flow
2) Delayed (15-30 min) osmotic effect → reduce brain water
What is the rate of axon regeneration?
1 mm per day
What are the muscles that are affected in masticatory myositis?
Temporalis
Masseter
Pterygoid
Describe the pathophysiology of acquired myasthenia gravis
The body starts to produce autoantibodies against the nicotinic acetylcholine receptors (AChR) at the neuromuscular junction of the skeletal muscles. These autoantibodies lead to compliment-mediated destruction of AChR, reduction of functional receptors, and decreased muscular responses to the acetylcholine release, which at the end impair the transmission of action potential from nerve to muscles and results in muscle weakness.
- This is a type II hypersensitivity
** There are 3 main mechanisms for loss of functional AChRs at the neuromuscular junction. The first involves complement-dependent lysis of the postsynaptic membrane caused by antibodies bound to AChRs and simplification of the postsynaptic membrane. Secondly, antibodies can cross-link AChRs on the surface of the membrane leading to increased internalization of AChRs, a decrease in the receptor half-life and decline of the total number of AChRs. In people, the half-life is reduced to 3 days from a normal of 10 days.9 Lastly, antibodies may directly inhibit AChR function.
Reference:
Textbook of Veterinary Internal Medicine,
Khorzad, R., Whelan, M., Sisson, A. and Shelton, G.D. (2011), Myasthenia gravis in dogs with an emphasis on treatment and critical care management. Journal of Veterinary Emergency and Critical Care, 21: 193-208. https://doi.org/10.1111/j.1476-4431.2011.00636.x
List 5 differentials for lower motor neuron diseases.
1) Acquired MG
2) Acute idiopathic polyradiculoneuritis
3) Tick paralysis
4) Elapid snake envenomination
5) Hypothyroidism
6) Paraneoplastic syndrome
What is the dose for Tensilon test?
Edrophonium is a short-acting anticholinesterase (last 10 minutes)
0.1-0.2 mg/kg IV
- Alternative: neostigmine 20 mcg/kg IV
Cholinergic crisis is a dangerous adverse effect from Tensilon test. Name 5 clinical signs and what is the recommended treatment?
Cholinergic crisis is acetylcholine overload at neuromuscular junctions secondary to inhibition of acetylcholinesterase
Clinical signs: hypersalivation, diarrhea, urination, increase bronchial secretion, bronchoconstriction, bradycardia, AV block, muscle twitching
* Patient can be in respiratory distress if the nAhR is overstimulated
Treatment: atropine 0.025 mg/kg IV
True or False: In dogs with acute idiopathic polyradiculoneuritis, cranial nerve usually is not affected; while in dogs with botulism, cranial nerve is often affected.
True
What type of bacteria cause tetanus?
Clostridium tetani
Gram (+), motile, noncapsulated, anaerobic, spore-forming bacteria
What are the two exotoxins for tetanus and how do they affect the body?
Tetanospasmin
- Binds to the membranes of the local motor nerve terminals → inhibits the release of neurotransmitter
Tetanolysin
- locally damaging viable tissue surrounding the infected area → optimizing the conditions for bacterial multiplication
What is the difference in the neurological signs between botulism and tetanus?
Botulism: flaccid paralysis
Tetanus: spastic paralysis
What is the difference in source between botulism and tetanus?
Botulism: contaminated food
Tetanus: contaminated wound, teething, parturition, OHE
What is the direction of infection in tetanus?
Motor → Sensory → autonomic nerve → spinal cord → brainstem
What type of interneuron does tetanus mainly affect?
Mainly affect inhibitory interneurons → inhibit release of GABA
List 10 clinical signs in Tetanus.
1) Lockjaw
2) Spasm of masticatory & pharyngeal muscles
3) Dysphagia
4) Hypersalivation
5) Opisthotonus
6) Erected ears
7) Wrinkled forehead (sardonic grin)
8) Third eyelid protrution & enophthalmos
9)
10)
What is the MOA of using magnesium in tetanus?
1) Non-specific Ca channel blocker → decreases Ca entry into presynaptic terminals → decreased
acetylcholine (ACh) release
2) Decreases the sensitivity of postsynaptic motor endplates to ACh
What neurological sign is the early indicator of Mg toxicity?
Deep tendon hyporeflexia (e.g. patellar tendon)
For dogs with tetanus, what is the poor prognosis?
Autonomic nerve involvement
Describe the severity classification for tetanus in dogs.
What are the three neurons coordinating the eyeball movements in respond to the vestibular signals?
CN 3, 4, 6
Where are the vestibular nuclei?
medulla oblongata
When would the paradoxical head tilt be seen?
1) Central vestibular diseases
2) Lesion at the cerebellar peduncle (flocculonodular lobe of the cerebellum or the supramedullary part of the caudal cerebellar peduncle)
Facial paralysis or spasm may be seen in dogs with peripheral vestibular disease, why?
Because CN 7 is very close to CN 8 and can be affected sometimes
True or False: Horner’s syndrome (oculosympathetic paresis) is one of the hallmarks for central vestibular disease.
False
Rarely seen in central vestibular disease but may be seen in peripheral vestibular disease.
Describe the Horner’s syndrome pathway.
Horner’s syndrome happens due to the loss of sympathetic nerve supply to the eye.
The entire pathway involves three neurons:
- First-order neuron: originates from hypothalamus descend to the midbrain and pons (ipsilateral) and terminates at the C8-T2 spinal cord
- Second-order neuron (pre-ganglionic neuron): Exits the T1 spinal cord and enters the cervical sympathetic chain, goes ascending and ends at the superior cervical ganglion (deep to the tympanic bulla) at C3-C4
- Third-order neuron (post-ganglionic neuron): Exits the superior cervical ganglion, follows the internal carotid artery and enter the cavernous sinus, joins the CN 6 and enter the orbits with CN 5
List 5 diseases that can cause Horner’s syndrome.
1) Brachial plexus injury
2) Severe middle/inner ear infection
3) Pneumothorax
4) First rib fractures
5) Idiopathic
6) Cervical trauma
What are the 4 signs of Horner’s syndrome
Ptosis
Miosis
Third eyelid protrusion
Enophthalmos
Which antibiotic can cause peripheral vestibular disease, which one can cause central vestibular disease?
Aminoglycoside - peripheral vestibular
Metronidazole - central vestibular
In a paper published in JVIM 2003 by Evans and colleagues, which drug can shorten the recovery time of metronidazole toxicity?
Diazepam 0.5 mg/kg PO q8h x 3 days (first dose is given as injection)
True or False: Glutamate + ammonia → Glutamine
True
Which cell in the brain facilitates the removal or ammonia?
Astrocytes
By transamination of glutamate into glutamine
List 3 excitatory neurotransmitter and 3 inhibitory neurotransmitter
Excitatory: Glutamate, aspartate, acetylcholine, epinephrine, norepinephrine
Inhibitory: GABA, serotonine, glycine
- Dopamine: modulation
Where does quinolinic acid come from?
Quinolinic acid is a strong excitatory neurotoxin (bind to NMDA receptors)
For cat with hepatic encephalopathy, which amino acid is essential in the diet?
arginine (important for urea cycle)
What are the three mechanisms for phenobarbital’s anti-seizure effect?
1) Prolong the opening of the Cl-channel associated with GABAa receptors
2) Inhibit glutamate receptor
3) Inhibit voltage-gated Ca channel
What is the phenobarbital’s protein binding capacity?
45%
After starting the phenobarbital, when should the patient be checked for serum drug level?
after 2 weeks (about 5 half-life so the drug can reach steady-state), and then after 6 weeks
What is the MOA of KBr as anticonvulsant?
Cause hyperpolarization of the neuron via Br influx through the Cl channels
How is bromide metabolized?
It is not metabolized and is excreted unchanged in urine
What is the half-life for KBr?
25 days
What is bromism and how do you treat it?
Bromide toxicity
Clinical signs: altered mentation, ataxia, upper or lower motor neuron paresis
Treatment: 0.9% NaCl
What is the MOA of zonisamide as anticonvulsant? What is the dose in dogs and cats?
Inhibition of voltage-gated Na channels
Inhibition of T-type Ca channels
Modulation of dopaminergic activity
Enhancement of GABA activity in the CNS
Inhibition of carbonic anhydrase activity
Dogs: 5-10 mg/kg PO q12h
Cats:10 mg/kg PO q24h
What is recommended therapeutic serum zonisamide level?
10-40 mcg/ml
What is MOA for levetiracetam?
Binding to the synaptic vesicle protein SV2A → decreased release of neurotransmitter into the synapse
GABA agonist
Ca channel antagonist
How is levetiracetam metabolized? What is the half-life?
minimal metabolism, mostly excrete in urine
Half-life: 3-4 hours
What is MOA of gabapentin?
Bind to the α2δ1 subunit of neuronal voltage-gated Ca channels → inhibition of release of excitatory neurotransmitters into the synapse
Which space does CSF locate?
Subarachnoid space
What are the 4 contraindications of CSF tap?
1) Acute traumatic brain injury
2) Coagulopathy or severe thrombocytopenia
3) Atlanto-axial luxation or cranial cervical vertebral fracture or luxation
4) Severe/rapidly progressing intracranial hypertension
List the tissue you will go through during CSF tapping.
1) Skin
2) Subcutaneous space
3) Muscles
4) Supraspinous ligament
5) Interspinous ligament
6) Ligamentum Flavum
7) Epidural space
8) Dura mater
9) Arachnoid
10) Subarachnoid space
What are the landmarks of CSF tapping at cisterna magna?
External occipital protuberance
C2 cranial edge of the spinal process
Dorsal arch of C1 vertebrae
Atlas wings
1) Draw a line between the external occipital protuberance and the C2 cranial edge of the spinal process. The spinal needle insertion site should be in the middle of that line
2) Draw a triangle between the external occipital protuberance and the two wings of atlas The spinal needle insertion site should be in the center of the triangle
How many ml of CSF can be safely removed in cats and small dogs? What about larger dogs?
Cats & small dogs: 1-2 ml
Larger dogs: 6 ml
What are the preferred lumbar CSF tap in large breed dogs, small breed dogs and cats?
Large breed dogs: L4 - L5
Small breed dogs: L5 - L6
Cats: L6 - L7
What is normal protein concentration and WBCs numbers in cisternal and lumbar CSF?
Cisternal: < 25 mg/dL, < 3/uL
Lumbar: < 40 mg/dL, < 5/uL
If there is RBCs in the CSF, how do you adjust the protein concentration based on the RBC number?
Every 1000 RBCs may increase protein concentration by 1 mg/dl
If there is RBCs in the CSF, how do you adjust the WBC count based on the RBC number?
Every 500 RBCs will increase WBC number by 1
What is the majority of WBC in normal CSF?
Small mononuclear cells (60-70%)
Large mononuclear cells (30-40%)
What is the dose of ketamine for dogs with refractory epilepsy?
5 mg/kg IV, followed by 0.1-0.5 mg/kg/hr
Which anticonvulsant is associated with pancreatitis?
1) Phenobarbital
2) KBr
3) Levetiracetam
4) Zonisamide
2) KBr
Which anticonvulsant is associated with necrotizing dermatitis and KCS?
1) Phenobarbital
2) KBr
3) Levetiracetam
4) Zonisamide
4) Zonisamide
What are the three CNs that are associated with dysphagia?
CN 9, 10, 11
What are the most common intracranial neoplasia?
Meningioma
What CN is affected when a patient has medial strabismus?
CN 6
Which CNs are purely sensory and which are pure motor?
Sensory: 1, 2, 8
Motor: 3, 4, 6, 11, 12
What is the most common CNS fungal infection in cats?
Cryptococcus
- Treatment: fluconazole
Where do the vestibular nuclei locate?
medulla/rostral medulla oblongata
What is the pathophysiology of paradoxical vestibular disease?
A subset of central vestibular disease
Because the cerebellum’s influence on the vestibular system is largely inhibitory, lesions in cerebellopontine angle cause vestibular release that is interpreted as a contralateral deficit. This results in clinical signs that are consistent with a lesion on the opposite side.
True or False: In paradoxical vestibular disease, the nystagmus fast phase will be directed towards the lesion; the head tilt will be away from the lesion; there can be ipsilateral deficits in CN V–XII; and postural reaction deficits is contralateral to the lesion.
False
Postural reaction deficits ipsilateral to the lesion
List 5 drugs that can cause ototoxicity
Aminoglycosides
Loop diuretics
Cisplatin
Chlorhexidine
Erythromycin
Chloramphenicol
Minocycline
What are the three types of disc herniation?
1) Hansen type I herniations: involve a complete rupture of the annulus with displacement of the nucleus into soft tissue structures.
2) Hansen type II herniations: ruptures of the inner layers of the annulus and only partial displacement of the nucleus into the annular fibers with annular hypertrophy
3) Non-compressive disk ruptures (also known as high-velocity low-volume, type III, traumatic) are small-volume herniations that result in significant spinal cord injury (e.g. ANNPE)
Describe central cord syndrome.
It’s a clinical presentation in which patients show more severe paresis in the thoracic limbs (TLs) than pelvic limbs (PLs).
In the more cranial cervical spinal cord (mainly C1-C5; some C6-T2), a midline disk herniation can cause compression of the more medial proprioceptive tracts associated with the thoracic limbs before compressing the most lateral belonging to the pelvic limbs.
- Hypoventilation indicates a poor prognosis
Which segment of the spinal vertebrae are most likely to develop diskospondylitis from migrating foreign body?
L2-L4
What is the common radiological findings on diskospondylitis?
Symmetrical lytic lesions of the adjacent vertebral endplates with reactive sclerosis and symmetric spondylosis
** Radiograph findings can lag from the clinical improvement
What is the main radiological difference between spinal tumor and diskospondylitis?
Most primary vertebral tumors involve one vertebral body and do not affect the IVD or cross the IVD space
What is the common empirical tx for diskospondylitis?
Cephalexin for 4-6 months to 1 year
How often for dogs with diskospondylitis develop subluxation?
20%
True or False: Phenobarbital is an auto-inducer of hepatic microsomal enzymes (p450 system), which can progressively decrease the elimination half-life with chronic dosing.
True
What is the recommended time to recheck KBr serum level?
6-12 weeks, and the annually
What will happen if you administer phenobarbital and zonisamide together long term?
Zonisamide’s half-life will decrease
List 10 metabolic causes of seizures.
Hypoglycemia
Hypothyroidism
Hypoadrenocorticism
Hyperbilirubinemia
Hypoxemia
Hyperosmolarity
Hyperthermia
Hyponatraemia and hypernatraemia
Hypocalcaemia and hypercalcaemia
Hepatic encephalopathy
Uraemic encephalopathy
Hyperlipoproteinaemia
What type of receptor is GABAb receptor? What happen when it is activated?
G- protein coupled receptor
Activation of GABAb receptor opens K channel and close Ca channels → hyperpolarization of the membrane.
Explain paroxysmal depolarization shift.
Sustained and uninhibited neuronal depolarization → Cellular influx of Ca → opening of voltage-gated Na channels and an influx of Na → burst of action potentials → plateau-like depolarization → rapid repolarization → hyperpolarization (mediated by GABA)
Define refractory status epilepticus and superrefractory status epilepticus.
Refractory status epilepticus: SE that does not respond to first-line anticonvulsant therapy.
Superrefractory status epilepticus: SE continuing or recurring more than 24 hours after initiation of treatment with anesthetic therapy.
Define status epilepticus.
Seizure activity that lasts > 5 minutes, or the occurrence of 2 or more seizures without recovery of consciousness.
What are the two main type of glutamate receptor. Which one does NMDA belong to?
Inotropic (influx of Na and Ca through the channel): NMDA, AMPA, kainate
Metabotropic (use a second messenger system to increase inward currents of Na & Ca, which leads to depolarization)
What happens when NMDA receptor is activated?
increase intracellular Ca → further depolarization
What are the two phases of SE.
1) Compensated SE
- Increase autonomic activity secondary to seizure activity
- hypertension, tachycardia, cardiac arrhythmias, hyperglycemia, hyperthermia, ptyalism, increased cerebral blood flow
2) Decompensated SE (after ~30 minutes of continuous seizure activity)
- Cerebrovascular autoregulation fails and intracranial pressure increases
- Hypoglycemia, hyperthermia, hypoxia, respiratory failure, acidosis, hyperkalemia, hyponatremia, uremia may occur
What is the onset of IV phenobarbital? What about keppra?
15 minutes
14 minutes
What are the three types of nerve injury?
1) Neurapraxia: mildest injury type and includes transient functional loss (conduction block) without loss of nerve continuity.
Axonotmesis: interruption of nerve axons with some degree of myelin loss. The surrounding perineurium and epineurium are preserved.
Neurotmesis: complete rupture of a nerve (axon, myelin, and surrounding structures). Recovery is not possible without surgical intervention
Benzodiazepine site on GABAa receptor
Between 𝛼 and 𝛾 subunits
How can cyproheptadine help in baclophen intoxication
Baclophen is an agonist of GABAb receptors –> opening of K+ channels –> hyperpolarization of cells
Cyproheptadine modulates the opening of the same Katp channel and also antagonises serotonin action which usually accumulates in baclophen intoxication
NMDA and AMPA collaboration
NMDA channel usually blocked by Mg, however when AMPA receptor binds to glutamate –> influx of Na –> positive cell –> Mg displaced –> NMDA can bind with glutamate and allow inflow of Ca++ which depolarises cell even more and also act as a second messenger for more synthesis of AMPA and NMDA receptors (long term potentiation)
NMB agents
depolarizing (short acting)
*succinilcolyne
non-depolarizing (intermediate acting)
* Benzyl
- Atracurium (histamine and laudanosine)
- Cisatracurium
* Aminosteroids
- Rocuronium
- Vecuronium
Reversal for NMB agents
Only for non-depolarizing
* neostigmine (AChesterase inhibitor) + atropine (when 10% TOF to counteract muscarinic sign)
*sugammex (incapsulates aminosteroids)
According to ACVIM status epilepticus consensus delineate the first, second, third and fourth line treatments
- first-line: benzodiazepines
- second-line: phenobarbital +/- levetiracetam +/- fosphenytoin
- third line: propofol +/- ketamine +/- dexmedetomidine +/- inhalant anaesthetics
- fourth line: neurostimulation
Cellular pathophysiology of SE
- NMDA and AMPA potentiation
- internalisation of GABA receptors
- overexpression of P-protein (drug efflux pump)
All of this leads to Ca++ neurotoxicity, apoptosis, cytotoxic and vasogenic oedema
Benzodiazepines MOA
- GABAa agonist
- reduced release of ACh
- Serotonin antagonist
Fosphenitoin
Inhibits Na and Ca influx
- NMDA and AMPA
this is the pro-drug of Phenytoin with less side effects
Primary vs secondary TBI
- primary is direct result of trauma:
- concussion
- contusion
- laceration
- secondary:
- systemic
- intracranial (excitotoxicity, ROS, NOS, glial cell involvement (TLRs, shift from M1 to M2 inflammatory phenotype) and vascular events (haemorrhage, BBB dysruption))
Poor prognostic factors for TBI
- no PLR
- low mGCS
- low HCT
- high BG
Corticosteroids are beneficial in spinal injury
Only methylprednisolone due to its free-radical scavenging properties, not pred or dexa
Most common organisms involved in diskospondilytis
- brucella
- asperigillus
- staph, street
- e.coli
