LIs For Mid-Semester Test Consolidation Flashcards
Encephalitis causes
- Infective (viral, bacterial, parasitic, fungal). Most are viral: herpes, Ross River, Murray River, rabies
- Autoimmune (aetiology unknown)
Infectious encephalitis clinical features, over time
- Initially, flu like: headache, fever, fatigue
- Later: stiff neck, confusion, seizures, loss of consciousness
Autoimmune encephalitis clinical features
- Memory loss
- Seizures (like infectious)
- Personality changes
Encephalitis investigations
- Brain imaging
- Lumbar puncture
- EEG
Encephalitis complications
For months/years+ afterward:
- Memory problems
- Persistent fatigue
- Hearing/vision problems
Can also result in coma and death.
Cerebral abscess causes (what kinds of infection?)
- Bacterial
- Fungal
Cerebral abscess clinical features
- Headache
- Fever
- Loss of consciousness
- Seizures
- Nausea/vomiting
Cerebral abscess investigations
- CT/MRI
- Blood tests for infection (CBC, ESR, CRP)
- Biopsy (rarer)
Cerebral abscess complications
Longer term:
- Neurological problems (e.g. memory, sensory, motor loss)
Can also result in death.
Stage vs grade of tumour — basic definitions
- Grade: appearance of the tumour cells; how well differentiated?
- Stage: size, location, and degree of spread.
What is the common grading system for tumour staging?
- TNM; Tumour, Nodes, Metastases
- Size/extent of tumour?
- Presence/extent of lymph node involvement?
- Presence/absence of metastases?
Recall the pnemonic for the different types of seizures
M CASTING (for mid-level actors):
M: Metabolic
C: Cortical malformation
A: Autoimmune
S: Stroke/vascular
T: Tumour
I: Infectious
N: Neurodegeneration
G: Genetic
Describe the vascular supply of the spinal cord. Where do each of these arteries originate?
- Anterior spinal: originates from two vertebral arteries, near their join
- Posterior spinal (2x): originates lower down the vertebral arteries
Which area of the spinal cord is supplied blood by which arteries?
Anterior 2/3: Anterior spinal artery
Posterior 1/3: Posterior spinal arteries
Explain how descending pathways from the brain can modulate spinal reflexes
- Can modulate directly, or indirectly (i.e. by altering interneuron activity)
- For instance, it can move your hand away from a hot object faster, or can inhibit reflexes when fine motor control is needed
How can proprioceptive feedback modulate reflexes?
- Golgi tendons/muscle spindles have their own reflexes, remember?
- They directly alter the activity of alpha motor neurons, influencing extrafusal muscle fibre contraction
What are the different kinds of intraocular muscle?
- Pupillary sphincter
- Pupillary dilator
- Ciliary muscle
CN III anatomical course
Exits brainstem ventrally, just caudal to the mammillary bodies. Heads up to eye, exiting skull through superior orbital fissure.
CN IV anatomical course
- Exits brainstem just caudal to the inferior colliculi
- Decussates, and heads up the ventral aspect of the brainstem
- Enters orbit via superior orbital fissure
CN VI anatomical course
- Emerges from pons, and travels up the ventral aspect of the brainstem
- Enters orbit through superior orbital fissure
CN V anatomical course
- Exits brainstem at mid-pons level
- Forms trigeminal ganglion, before branching off into V1, V2, and V3
- V1: Opthalmic (superior orbital fissure)
- V2: Maxillary (foramen rotunda)
- V3: Mandibular (fossa ovalis)
(Note: motor components joins V3, which is why it is bigger and hence oval shaped)
(Three nuclei: mesencephalic, pontine, spinal)
CN VII anatomical course
- Many, many brainstem nuclei
- Emerges at pontomedullary junction
- Exit skull via internal auditory meatus
- Sensory and para. exit facial canal
- Motor exits via stylomastoid foramen (what are its areas of the face?)
CN III function
Motor: Extraocular muscles (incl. levator palpebrae superioris; minus sup. oblique and lateral rectus)
Parasympathetic: Pupillary sphincter muscle (inner). Accommodation (ciliary muscle)
CN IV function
Motor: Controls contralateral superior oblique
CN V Function
Motor: pterygoid, temporalis, mandible (mastication)
Sensory: touch, temperature, pain, and proprioception of face, mouth, nasal cavity, and cranial dura
CN VI function
Motor: ipsilateral lateral rectus
CN VII function
Motor: muscles of facial expression (what are the five branches?)
Parasympathetic: parotid glands
Sensory: external auditory meatus, tympanic membrane, and external ear (pinna)
Special sensory: taste on anterior 2/3 of tongue
Explain the difference in patience presentation between bells palsy and stroke
Bell’s Palsy: not able to move eyebrow, distal to decussation. Linked to nerve damage.
Stroke: damage occurs within brain parenchyma, upstream from decussation. Ipsilateral lower facial motor loss. Worse.
CN III palsy
- Eye is down and out (two remaining muscles)
- Pupil is dilated (no para. input)
- Eyelid is drooped (no levator palpebrae superioris)
CN IV Palsy
- Eye is deviated upward inward (no superior olbique)
- Compensatory head tilt away from affected eye
CN V Palsy
- Sensory loss in face, ant 2/3 of tongue, cranial dura
- Motor loss in muscles of mastication (what are they?)
- When mouth is opened, jaw deviates towards affect side
CN VI Palsy
- Eye is deviated inward (no lat. rectus)
- Diplopia
CN VII Palsy
- Motor loss in face
- Loss of salivation/tongue sensation if proximal to splitting of CN VII (parotid is preserved)
CN VIII Function
Special Sensory: Balance and hearing
CN IX Function
Motor: Minor role in elevating larynx and pharynx during swallowing
Para.: Parotid glands
Sensory: Anterior 2/3 of tongue
Special Sensory: Taste of anterior 2/3 of tongue
Visceral Sensory: Carotid bodies
CN X Function
Motor: Pharynx, soft palate, and larynx (speaking and swallowing)
Para: Heart, GI tract, trachea
Sensory: Larynx and laryngopharynx
Special Sensory: Taste at root of tongue
CN XI Function
Motor: Upper Trapezius and SCM
CN XII Function
Motor: Extrinsic (positioning) and intrinsic (movement) muscles of tongue
CN VIII anatomical course
- Arises from vestibular nuclei and cochlear nuclei (bipolar)
- Leaves skull at internal acoustic meatus
- Cell bodies found in spiral (hearing) and vestibular (balance) ganglia; other pole synapses on cochlea/vestibular apparatus separately
CN IX/X anatomical course
- Arise from a series of many brainstem nuclei
- Exit skull and connect with effector after leaving the skull through the jugular foramen
CN XI anatomical course
- Spinal portion arises from C1-C5
- Cranial portion joins CN X
- Enters via foramen magnum; exits via jugular foramen
CN XII anatomical course
- Arises from hypoglossal nucleus in medulla
- Exits skull via hypoglossal canal
CN VIII palsy
- Nystagmus
- Tinnitus
- Vertigo
- Sensorineural hearing loss
Which nerves control the sensory/motor arms of the gag reflex
Sensory: CN IX
Motor: CN X
CN IX/X palsy
Uvula deviates away from affected side when (say “aah”)
Peripheral vs central vertigo
Peripheral: Inner ear/vestibular nerve
Central: Brain/Brainstem
Causes of central vertigo
Vascular:
- Posterior circulation stroke
- Vertebrobasilar insufficiency (usually atherosclerotic)
Other:
- Multiple sclerosis
- Tumour
Causes of peripheral vertigo
- Benign paroxysmal positional vertigo
- Meniere’s disease (triad; vertigo, tinnitus, sensorineural hearing loss)
- Vestibular neuronitis/labrynthitis
What are some causes for non-vertiginous dizziness?
Cardio:
- MI
- Arrhythmia
- Aortic stenosis
- Pulmonary embolism
Neuro:
- Normal pressure hydrocephalus (remember the lady who fell over while gardening?)
Other:
- Hypoglycaemia
- Drug related
Describe the presenting features of Benign paroxysmal positional vertigo
Recurrent, brief attacks of positional vertigo.
Explain the pathophysiology of primary open angle glaucoma
- Increased resistance to outflow of aqueous humour from the trabecular meshwork
- Increased intraocular pressure
- Retinal ganglion cell death (and therefore optic neuropathy)
Explain the pathophysiology of acute angle closure glaucoma
- “Pupillary block”
- Lens pushes out on iris, decreasing the angle of the trabecular meshwork
- Decreased aqueous humour outflow
- Increased intraocular pressure
- Ganglion cell death (and therefore optic neuropathy)
What is the common thread amongst all “Glaucoma”s?
A group of diseases whereby vision is lost due to damage of the optic nerve.
Guillain Barre symptoms
- Classically: ascending weakness
- Paraesthesia in fingers/hands/toes/feet
- Respiratory issues (if resp muscles affected)
- Facial weakness/sensory loss (remember: CNs are part of the peripheral nervous system)
- Autonomic dysfunction
What are some possible causes of GBS?
- Viral infection (e.g. EBV)
- Bacterial infection (e.g. camylobacter jejuni)
- Vaccination
- Surgery
(?Molecular mimicry)
GBS investigations
- Lumbar puncture
- EMG
GBS lumbar puncture results
Increased protein; normal white blood cell count.
GBS EMG findings
Abnormal nerve conduction (makes sense)
GBS treatment
- Intubation/ventilation if required
- Plasmapheresis (filter out plasma, and therefore autoantibodies)
- IvIg; introduction of healthy antibodies to dilute autoantibodies
Complications of GBS
- Respiratory muscle paralysis (respiratory failure/pneumonia)
- DVT leading to PE (immobilization)
Broadly, describe prion diseases
- Prions are a type of protein that can trigger normal proteins to fold abnormally.
- Prion diseases refer to the accumulation of these prions in the brain (e.g. CJD = Mad cow disease)
Describe the three classes of structural filaments in a neuron, and their functions
- Neurofilament (main structural protein)
- Microtubule (cellular transport pathway)
- Actin filament (regulates neuronal shape change)
What investigations do we perform in a patient who has lost consciousness?
- Bloods (EUC/LFT, creatinine; kidney, glucose; hypoglycaemia)
- Blood gas (check for respiratory failure)
- CXR
- ECG (cardiac causes)
- CT/MRI of head (tumour/stroke/herniation/haemorrhage etc.)
- Lumbar puncture (infection)
- Toxicology
Describe the role of SCI rehabilitation
- Return patient to highest level of function possible
- Help assist with activities of daily living; as independent as possible
- Support family, make adjustments to living environment
Only lesions proximal to the ___ can cause unilateral hearing loss. Why?
- Proximal to the cochlear nuclei
- This is because, once the nerves reach the ventral and dorsal cochlear nuclei, projections are bilateral
What are the dorsal cochlear projections responsible for? Describe the pathway.
- Responsible for quality of sound
- Cochlear nerve synapses on dorsal cochlear nuclei
- Crosses at pontine tegmentum, and ascends in lateral lemniscus (not medial, which is DCML)
- Synapses on inferior colliculus
- Passes through brachium of inferior colliculus, and heads to MGN of thalamus
- Then to primary auditory cortex
What are the ventral cochlear projections responsible for? Describe the pathway.
- Responsible for timing of sound
- Cochlear nerve synapses at ventral cochlear nuclei
- Fibres continue bilaterally (some crossing at trapexoid body) to superior olivary nucleus (remember climbing fibres? they’re just downstairs in the inf. olivary nucleus)
From here, pathway is same as dorsal:
- Lateral lemniscus to inferior colliculus
- IC brachium to MGN of thalamus
- Primary auditory cortex
Draw the direct/consensual light reflex pathway
https://lh3.googleusercontent.com/proxy/f5wJ0AZeLB_wsTHeLiliVVh3QjE2KM35XjnUfxIqlJlz8W1GwExUEu-2eh-xyCnbOLw4r7OwSepAfbmYhoXhhL-JqvmH7GtvVMOWYcoKXz4NMyu0loP-AAiwYs3lIReq_eJKpixgzKcf4VbB
What is another name for the piriform cortex?
Primary olfactory cortex!
