Neurology COPY Flashcards
What creates the resting membrane potential of a neuron?
- Na/K ATPase pumps: exchange 3 Na+ ions out of the cell in exchange for 2 K+ ions
- Creates a more negative potential inside the cell compared to the outside
What is the resting membrane potential difference of a neuron (in mV)?
-65 to -70 mV
What triggers opening or closing of the ion channels in a neuron?
Membrane voltage or a neurotransmitter binding to a receptor linked to the channel
When a neuron depolarizes past -55 mV, what channels open to begin the action potential?
Voltage gated Na+ channels
As Na+ diffuses into the cell, it further depolarizes the membrane until it approached the equilibrium potential for Na+. What is this (in mV)?
59 mV
The depolarization of the membrane from Na+ influx triggers the opening of voltage-gated K+ channels. What occurs?
K+ diffuses out of the cell to its equilibrium potential of -90 mV
How do toxins such as pyrethrins cause tremors and seizures?
Block sodium channel inactivation, increasing action potential generation
What two factors influence the speed at which action potentials travel down an axon?
- Axonal diameter
- Myelin
Ions flow directly between neurons in what types of synapses?
Electrical synapses or gap junctions
What causes the release of neurotransmitters into the synapse?
- Action potential depolarizes the nerve terminal => opening of voltage gated Ca++ channels
- Ca++ flows into the cell and activates synaptic vesicle proteins that allow the vesicle to dock and fuse with the cell membrane => release of the neurotransmitter into the synaptic cleft
Name 3 families of ionotropic receptors
- Nicotinic acetylcholine, gamma-amino butyric acid (GABA) and glycine
- Glutamate
- ATP or purine P2X receptors
What occurs when acetylcholine binds to nicotinic receptors?
The nicotinic pore becomes permeable to cations => Na+ diffusion into the cell => depolarization of the post-synaptic neuron
What enzyme in the synaptic cleft breaks down acetylcholine to choline and acetic acid?
Acetylcholinesterase
What causes myasthenia gravis?
Autoantibodies against the alpha1 subunit partially block the acetylcholine receptor in the neuromuscular junction
What is the major inhibitory neurotransmitter? What occurs when the receptor is stimulated
- GABA
- The GABA-A receptor becomes permeable to Cl-, leading to diffusion of Cl- into the cell
- Leads to hyperpolarization of the cell and an inhibitory post-synaptic potential
What is the mechanism of action of diazepam and phenobarbital?
Bind to the extracellular sites on the GABA-A receptor - do not open the channel, but they alter the kinetics so that it stays open longer after GABA binds. Makes it harder to depolarize the cell and cause seizures
What is the major excitatory neurotransmitter in the CNS? What are the two receptors it binds to?
- Glutamate
- AMPA and NMDA - must bind both receptors to produce an effect
What happens after glutamate binds AMPA and NMDA?
- Binding to AMPA partially depolarizes the membrane and releases a Mg++ ion that was blocking NMDA
- Binding to NMDA then leads to additional Na+ and Ca++ conductance
What causes excitotoxicity?
Excessive NMDA receptor activation, leading to accumulation of intracellular Ca++ => cell death
A system of microtubules is utilized for transporting proteins, vesicles, etc from the neuronal cell body to the axon and back. What are the names of these microtubules?
- Kinesins - transport from the cell body to the axon terminal
- Dyneins - transport from the terminal back to the cell body
What is temporal summation?
Several action potentials from the same pre-synaptic neuron summate to depolarize the post-synaptic neuron
What is spatial summation?
Several action potentials from multiple, different pre-synaptic neurons summate to depolarize the post-synaptic neuron
What is the reticular activating system?
- Monoaminergic and cholingeric neurons in the brainstem and basal forebrain send large projections to activate the forebrain and mediate consciousness, attention, etc.
- Lesions within these projections can lead to stupor or coma
A head or body turn typically localizes disease to what region?
Rostral brainstem or cerebral disease
A plantigrade stance localizes disease to what?
Peripheral neuropathies
Describe decerebrate rigidity. Where does this localize disease to?
- Opisthotonus with rigid extension of the neck and all four limbs
- Midbrain or rostral cerebellar lesions
Describe decerebellate rigidity. Where does this localize disease to?
Opisthotonus with extension rigidity of the limbs BUT the hips are flexed or intermittently flexed
- Severe cerebellar lesions
A short, choppy, stilted gait is often indicative of what type of paresis?
Lower motor neuron
A long-striped, spastic gait with proprioceptive ataxia is indicative of what type of paresis?
Upper motor neuron
What causes general proprioceptive ataxia?
Disruption of the spinocerebellar tracts and conscious proprioceptive pathways that relay the anatomic location and degree of muscle contraction to the brain
Describe what general proprioceptive ataxia looks like
- Crossing the limbs
- Scuffing or dragging the digits
- Standing or landing on the dorsal aspect of the paws
- Delay in the swing phase of the gait
What causes vestibular ataxia?
Loss of orientation of the head with respect to the eyes, neck, limbs, and trunk
Describe what vestibular ataxia looks like
- Tendency to drift, lean, or fall in one direction
- +/- head tilt or nystagmus
- Normal strength and proprioception with peripheral lesions, may be abnormal with central lesions
Describe what cerebellar ataxia looks like
- Hypermetric gait with sudden bursts of motor activity
- Overflexion of the limbs on protraction
What must be intact for a pet to perform postural reactions?
All major sensory and motor (UMN and LMN) components of the CNS and PNS - using postural reactions to evaluate conscious proprioception is a misnomer, because all postural reactions rely on BOTH motor and proprioceptive systems
What is the prosencephalon?
Cerebrum and thalamus
Unilateral prosencephalic lesions (cerebrum and/or thalamus) will result in postural reaction deficits on what side? They are usually accompanied by what other changes?
- Contralateral side to the lesion
- Often accompanied by contralateral menace deficit, contralateral sensory deficits, or changes in mentation/behavior
- Gait is usually normal but may circle or pace
Describe the characteristic physical exam findings with a T3-L3 lesion
- Postural reaction deficits in the pelvic limbs with normal thoracic limbs
- Paraparesis with GP ataxia
- UMN in the pelvic limbs: normal to exaggerated muscle tone and spinal reflexes
Describe the characteristic physical exam findings with a C1-C5 lesion
- Tetraparesis with GP ataxia
- Postural reaction deficits in all four limbs
- UMN signs in all four limbs - normal to exaggerated spinal reflexes and muscle tone
+/- Horners syndrome
+/- respiratory difficulty
Describe the characteristic physical exam findings with a C6-T2 lesion
- Thoracic limbs: LMN signs - flaccid paralysis or paresis, short choppy gait, reduced withdrawal reflexes and muscle tone
- Pelvic limbs: UMN signs/GP deficits - long strided gait, normal to exaggerated spinal reflexes and muscle tone
- +/- Horners with T1-T3 lesions
What mediates the patellar reflex?
Femoral nerve through the spinal cord segments L4-L7
In the thoracic limbs, the nerves responsible for the withdrawal reflex arise from what spinal cord segments?
C6-T2
In the pelvic limbs, the nerves responsible for the withdrawal reflex arise from what spinal cord segments?
Mediated by the sciatic nerve through L6-S1
With spinal cord lesions, where will the cutaneous trunk reflex stop?
Typically it is preserved for 1-2 vertebral bodies caudal to the level of the lesion
Deficits in cranial nerve III will lead to what clinical signs?
Oculomotor nerve = motor to the extraocular muscles and parasympathetic to the pupil
- Ventrolateral strabismus
- Diminished to absent PLRs with dilated pupils
Deficits in cranial nerve IV will lead to what clinical signs?
Trochlear nerve = motor to the dorsal oblique muscle
- Dorsomedial strabismus
Deficits in cranial nerve V will lead to what clinical signs?
Trigeminal = motor to the muscles of mastication, sensory to the face
- Masticatory muscle atrophy, dropped jaw if bilateral
- Decreased or absent facial sensation
Deficits in cranial nerve VII will lead to what clinical signs?
Facial = motor to muscles of facial expression, parasympathetic to lacrimal glands, taste
- Inability to close the eyelid, move ear, or retract lip
- Hemifacial tetany
- Dry eye
Deficits in cranial nerve VIII will lead to what clinical signs?
Vestibulocochlear = balance, hearing
- Head tilt, vestibular ataxia, nystagmus
- Deafness
Deficits in cranial nerve IX will lead to what clinical signs?
Glossopharyngeal = sensory and motor to the pharynx
- Diminished gag reflex, dysphagia
Deficits in cranial nerve X will lead to what clinical signs?
Vagus = sensory and motor to the pharynx, larynx, and viscera
- Diminished gag reflex, dysphagia
- Laryngeal paralysis
- Megaesophagus
The menace response may be absent until what age in puppies and kittens?
10-12 weeks
What must be intact for the menace response to occur?
- Functional optic nerve (CN II)
- Optic tract (diencephalon)
- Optic radiation up to the occipital cortex
- Functional cerebellum
- Efferent pathway to the facial neurons (CN VII)
Deficits caudal to the optic chiasm will result in an absent menace on what side?
Contralateral side
What must be intact for a pupillary right reflex to occur?
- Functional optic nerve (CN II)
- Intact optic tract (thalamus)
- Optic radiation up to the occipital cortex
- Functional oculomotor nerve (CN III)
If a patient has an absent direct PLR but a positive indirect PLR in one eye, where is the lesion?
In the eye itself or the optic nerve on that side
What must be intact for palpebral reflex to occur?
CN V and VII
What must be intact for physiologic nystagmus to occur?
- Vestibulocochlear (CN VIII) relays impulses to the brainstem
- Abducent (VI) and oculomotor (III) neurons => abduction and adduction of the eyeball
What is Schiff-Sherrington sign? It occurs with lesions in what portion of the spinal cord?
- Spastic paraplegia in the thoracic limbs with either UMN signs or paradoxical LMN signs in the pelvic limbs
- Occurs with T3-L3 lesions
What gene leads to dramatically accelerated intervertebral disc degeneration in chondrodystrophic breeds?
Expression of fibroblast growth factor 4 (FGF4) on chromosome 12
In Hansen type I IVDE, what changes occur in the nucleus pulposus that lead to failure of the intervertebral disc unit and extrusion of mineralized material into the vertebral canal?
Early chondroid metaplasia, degeneration, and mineralization
What is the nucleus pulposus?
The highly hydrated central portion of the disc
What is the annulus fibrosis?
The ligament that makes up the periphery of the disc and attaches to the vertebral endplates
What characterizes Hansen type II IVDE?
Protrusion of the annulus fibrosis - fibroid metaplasia leads to slow protrusion of the disc into the spinal canal. Annulus remains intact (nucleus pulposus does not extrude out)