Neuro Written Exam Qs Flashcards
What are the different ways seizures can be classified?
-
Partial/focal → affect a single area of the brain, can have secondary generalisation
- simple partial: consciousness intact
- complex partial: loss of consciousness
-
Generalised – diffuse activity across the entire brain
- absence: sudden lapse in awareness
- myoclonic: sudden single jerks of muscles
- tonic-clonic: alternating stiffening and jerking
- tonic: stiffening
- atonic: “drop” seizures
What are the different medications that can be used to manage epilepsy? Describe their MOA and some side effects
General concepts for treatment:
- most common first line drug is valproate except in women of childbearing age due to teratogenic effect, carbamazepine is often used instead
- ethosuximide for absence seizures
- Blocking VGSCs
- reduces AP transmission
- Eg: Phenytoin (2nd line for adults & 1st line for kids), Na Val (1st line), Carbamazapine (if PREGGO, then can’t use Na Val. Also high s/e for skin rash & SJS)
- Blocking VGCCs
- inhibit neurotransmitter exocytosis
- Eg: Gabapentin, Pregabalin, Ethosuximide (absent seizure)
- GABA agonist
- Increasing GABAergic activity
- Eg: Benzodiazepines (diazepam, midazolam), barbiturates
- GABA Transaminase Inhibitor
- Reducing breakdown of GABA
- eg valproate and vigabatrine
Side Effects ⇒
- General (for all) →
- CNS - dizziness, headache, blurred vision
- GI - nausea, vomiting, diarrhea, weight gain
- Motor - EPSE (reversible), ataxia
- Allergy - SJS/anaphylaxis particularly for Lamotrigine & Carbamazapine
- Specifics:
- GABA inhibitor - respiratory depression
Describe the path CSF takes from the choroid plexus in the lateral ventricles to when it returns to the venous system
- CSF in lateral ventricles → third ventricle via interventricular foramen
- Third ventricle → fourth ventricle via cerebral aqueduct (of Sylvius)
- fourth ventricle → cisterna magna (via median aperture (of Magendie) and cerebellopontine cisterns (two lateral apertures (of Luschka).
- some CSF flows through the obex and enters the central canal of the spinal cord
- CSF flows through the subarachnoid space of the brain and spinal cord
- CSF reabsorbed into the dural venous sinuses via arachnoid granulations
What are the causes of meningitis (include common pathogens)
meningitis = inflammation of the meninges
encephalitis = inflammation of brain parenchyma
Routes of transmission:
- haematogenous
- crossing blood-brain barrier = encephalitis
- crossing blood-CSF barrier = meningitis
- direct spread from adjacent sites such as the sinuses, mastoid, skull fractures
- iatrogenic
- neural spread of viruses
Pathogens
- Bacteria:
- Most common: Neisseria Meningitidis (causes meningococcal), S. Pneumoniae
- Less common: H. Influenzae, Group B Stap
- Virus: HSV, HIV, adenovirus, EBV
Staph & strep ⇒ gram positive
E.coli, the rest ⇒ gram neg
What are the common signs and symptoms of meningitis
positive Kernig’s sign:
- flex hip and knee 90°
- extension of the knee should be difficult/painful
positive Brudzinski’s sign:
- passive flexion of the neck results in flexion of the knee/hip
QUAD of Danger:
- Headache
- Photophobia
- Neck stiffness (nuchal rigidity)
- Non-blanching rash → belly
Fill out the following table below comparing bacterial and viral meningitis on lumbar puncture results
Describe the normal pathways involved in horizontal conjugate gaze (for example for a person looking to their right)
Normal conjugate gaze pathway
frontal eye field activated → decussates at pons → contralateral PPRF → CN VI (of the PPRF side) → abduction + MLF of the other side (the same side as the side where FEF got activated) → CN III of the FEF side → adduction of the other eye
- looking to the right
* Left FEF → decussates at pons → R) PPRF → CN VI → R) eye abduction + activation of L) MLF → L) MLF activates L) CN III → L) eye adduction → conjugate gaze to the right - looking to the left
* Right FEF → decussates at pons → L) PPRF → L) CN VI → L) eye abduction + R) MLF activation → R) CN III → R) eye adduction → conjugate gaze to the left
What is the difference in presentation/location of the lesion between one and half syndrome and INO
INO
- In INO, the lesion is on the MLF. Therefore, the ipsilateral MR does not contract -> can’t adduct.
- It’s named ipsilaterally (Left MLF damage → Left INO → Left MR cant contract when looking to the right)
- Good eye can abduct but with nystagmus.
- Can be bilateral in MS
One and a half syndrome
- In one and a half syndrome, the lesion PPRF & MLF of the same side -> ipsilateral gaze palsy -> defective ipsi adduction + normal contra abduction with ataxic nystagmus
Outline the steps in the pupillary light reflex
You shine a torch into the patient’s left eye: there is no direct or consensual response. When you shine the torch into the right eye, there is a direct and consensual response. Where is the lesion most likely?
Left optic nerve
Outline the visual pathway from the retina to the visual cortex, include the effects on vision of different lesions along the pathway (eg at the optic chiasm)
Light → photoreceptors → retinal ganglion → optic disc → optic nerve → optic chiasm → optic tract → LGN (primary - standard vision) / superior colliculus (secondary pathway - rapid eye movement/reflex) / hypothalamus and brainstem (tertiary pathway - in circadian rhythm) → superior & inferior optic radiation → V1 → we process what we see
Eyeball defect:
- Central scotoma - damage to optic disc - blind in the central middle
- Mono-ocular blindness - dmg to optic nerve
- Bitemporal hemianopia - dmg to optic chiasm
- Homonymous hemianopia - dmg to optic tract
- Superior quadrant-anopia - dmg to inferior optic radiation (medial side)
- Inferior quadrant-anopia - dmg to superior optic radiation (lateral side)
- Homonymous hemianopia (radiation) - dmg to both superior + inferior optic radiation
- Homonymous hemianopia with macular sparing - V1 is damaged
Draw the following pathways and explain their function:
Corticospinal tract (lateral + anterior)
Corticospinal tract (lateral + anterior) - descending - for movement of axial & appendicular skeleton
carries motor signals from M1/SMA/PMA to LMNs in the spinal cord
- primary neuron is an UMN originating in the motor cortices
- travels down through internal capsule – genu and anterior portion of posterior limb (FAL)
- decussation of some fibres at the pyramidal decussation creates two pathways
- lateral CST: 90% of fibres decussate in medulla and continue contralaterally in lateral SC. Distal or appendicular muscles
- anterior CST: 10% of fibres remain ipsilateral and continue down in the anterior SC before later. Proximal or axial muscles decussating at the level they innervate via the ventral white commissure
- synapse onto secondary neuron which is LMN in the ventral horn of the spinal cord
Draw the following pathways and explain their function:
Corticobulbar tract
Corticobulbar tract - descending - head & neck innervation
carries motor signals from M1/SMA/PMA to LMNs in motor cranial nerve nuclei (5,7, 12, 11, NA(9,10))
- primary UMN from motor cortices travels down through genu of internal capsule
- synapse onto secondary LMN in motor cranial nerve nuclei, most of these nuclei are supplied bilaterally from the left/right CBT with two exceptions
- facial: upper facial nuclei have bilateral innervation, lower nuclei contralateral only
- hypoglossal: primarily contralateral innervation
Draw the following pathways and explain their function:
Dorsal column medial lemniscus
Dorsal column medial lemniscus - ascending - vibration, fine touch, proprioception
major sensory pathway for fine and discriminative = touch (meisnner’s), ruffini(vibration) and proprioception
- primary sensory neurons with cell bodies in dorsal root ganglia enter the spinal cord through the dorsal roots and form the ascending dorsal columns (gracile/cuneate fasciculi)
- synapse onto secondary neurons in dorsal column nuclei of medulla (cuneate and gracious nucleus)
- secondary neurons decussate as the internal arcuate fibres before travelling up to the thalamus as the medial lemniscus
- synapse onto tertiary neurons in the VPL nucleus of the thalamus which continue up to S1
Spinothalamic tract
Spinothalamic tract - ascending - pain & temp
Sensory pathway for pain and temperature
- primary sensory neurons with cell bodies in dorsal root ganglia enter spinal cord via dorsal roots and synapse in dorsal horn at same level (or slightly above/below via Lissauer’s tract). DRG enters the spinal cord in the rexed lamina area
- secondary neuron immediately decussates through ventral white commissure and ascends in the STT of the lateral funiculus
- synapse onto tertiary neuron in the VPL nucleus of the thalamus before continuing to S1
fibres within the STT also have a number of additional cortical connections
- reticular formation – alertness due to pain
- Midbrain/spinomesencephalic – periaqueductal grey for descending pain modulation
- hypothalamus – SNS response to pain
- limbic system – emotional response to pain
- Spinotectal (sup colliculus - vision)
Explain the basic function of the following pathways:
Extrapyramidal tracts – reticulospinal, rubrospinal, tectospinal, vestibulospinal
vestibulospinal – vestibular nuclei project to spinal cord for balance/posture
o medial for bilateral head/neck control
o lateral for ipsilateral proximal muscles
· reticulospinal – two opposing pathways ipsilaterally control lower limb posture/walking
o pontine/medial activates extensors
o medullary/lateral inhibits extensors
· rubrospinal – from red nucleus, complementary pathway to CST with unclear role
· tectospinal – superior colliculus projects to SC to coordinate head/neck in visual reflexes
Spinocerebellar tract
unconscious proprioception involved in cerebellar function
- primary sensory neurons synapse in dorsal horn of spinal cord
- secondary neurons ascend to ipsilateral cerebellum via two pathways:
- information from golgi tendon organs travel up ipsilaterally through dorsal SCT and inferior cerebellar peduncle. Clarke’s nucleus is c8-l2/l3 which is imp for Dorsal SCT.
- information from muscle spindles decussates and ascends through the ventral SCT contralaterally before decussating again in the brainstem and entering the ipsilateral cerebellum via the superior peduncle
Extra -> cuneate SCT. Dorsal horn -> straight to medulla accessory cuneate nucleus -> 2nd order neuron -> through the inferior cerebellar peduncle -> cerebellum
Trigeminothalamic tract
sensory information from the face
- primary sensory neurons with cell bodies in trigeminal ganglia enter the brainstem and synapse in one of three sensory nuclei
- mesencephalic (midbrain): proprioception
- principal sensory nucleus (pons): fine touch
- spinal trigeminal nucleus (medullar): pain and temperature
Explain the difference in presentation between Bell’s palsy and a stroke affecting the corticobulbar tract
Bell’s palsy - CN VII is affected - ipsilateral paralysis of the muscles innervated by CN VII and also:
- Loss of taste on ipsilateral affected side
- Dry mouth
- Hyperacusis - due to stapedius muscle palsy (innervated by CN VII)
Corticobulbar tract - contralateral paralysis of the lower facial muscles because:
Upper facial nuclei - bilateral innervation
Lower facial nuclei - contralateral only
Draw the direct and indirect motor loops of the basal ganglia
basal ganglia play a key role in motor planning and modulation of movement, the initiation and termination of a movement program is determined by two parallel pathways which are activated/deactivated by neurotransmitters in the striatum acting on medium spiny neurons
- direct pathway – initiates movement, increased dopamine from SNpc
- indirect pathway – terminates movement, increased ACh from within striatum
DIRECT PATHWAY
activated due to dopamine from SNpc activating D1 neurons and inhibiting D2 neurons
- excitatory signals descends from motor cortex to D1 neurons
- D1 neurons inhibit the GPi/SNpr by releasing GABA
- reduces inhibition by the GPi/SNpr on the PPN and thalamus
- increased output from PPN (pedunculopontine nucleus) and thalamus resulting in greater SC output
INDIRECT PATHWAY
activated due to ACh from large aspiny striatal neurons activating D2 neurons via M1 receptors and inhibiting D1 neurons via M2 receptors
- excitatory signal descends from motor cortex to D2 neurons
- D2 neurons inhibit the GPe
- reduces inhibition by the GPe on the STN
- increased excitatory output from STN on the GPi/SNpr
- greater inhibition from GPi/SNpr on thalamus and PPN
- decreased output from PPN and thalamus results in diminished SC output
Explain the pathophysiology of Parkinson’s disease and Huntington’s disease.
Parkinson’s disease – unclear cause results in degeneration of dopaminergic neurons in the SNpc leading to a shift towards ACh in the striatum and the indirect pathway
- major clinical signs: bradykinesia, rigidity, resting tremor
- pharmacological management delayed as much as possible, mainstay is levodopa + carbidopa to restore dopamine in the striatum while limiting peripheral excess
Huntington’s disease – neurodegenerative disease that primarily affects GABAergic neurons of the indirect pathway and cholinergic aspiny neurons of the striatum
- occurs due to autosomal dominant mutation in the huntingtin protein resulting in CAG repeats that produce a polyglutamine tail in the dysfunctional gene product
- clinical signs: chorea, decreased muscle tone
- managed with antipsychotics, antidepressants, counselling/support
You see a patient in the ED who speaks to you in a monotonous voice and no emotions about recently seeing a UFO land in his backyard. He tells you that no one believes him and that they are here to take him back to the mother ship.
- What is the DSM V criteria for schizophrenia?
- You must have 2 out of the 5 s/s of schizo, and 1 of them must be positive symptoms
- All s/s must be persistent for at least 6 months with positive symptoms >1month
- Must have significant impact to ADLs (dysfunctional life)
Sign & Symptoms
- Positive
- Hallucination - auditory, visual, smell (unreal)
- Delusion - false belief
- Speech disturbances/ disorganization
- Thought disturbances
- Negative - 5A+C
- Anhedonia
- Alogia
- Avolition
- Asocia
- Affect flat
- Catatonia
What are 5 risk factors for a person developing Schizophrenia?
Modifiable - substance use/abuse
Non modifiable - genetics, FHx, obstetric complications, childhood trauma, paternal age, 2nd generation immigrant, urban upbringing
You see a patient in the ED who speaks to you in a monotonous voice and no emotions about recently seeing a UFO land in his backyard. He tells you that no one believes him and that they are here to take him back to the mother ship.
How would you treat this patient?
- MSE
- Investigations to rule out organic causes (bloods, xray, ctb, etc)
- Medical, family, psych history
- Modification of pre existing tx if any
- If new onset - ?start on antipsych to stabilise psychosis
- multiD approach with psych team
What are the components of an MSE?
ABS MAT PCI JR
Appearance
Behaviour
Speech
Mood
Affect
Thought form
Thought process
Perception
Cognition
Insight
Judgement
Risk assessment
What are 2 typical and 2 atypical antipsychotics? What are their mechanism of action?
Typical
- 1st gen
- D2 receptor antagonist - almost complete inhibition of D2 receptor
- Eg: haloperidol, chlorpromazine
Atypical
- 2nd gen
- D2 receptor antagonist and serotonin receptor antagonist
- Eg clozapine, olanzapine
What are 5 side effects of antipsychotics? What is the difference between the side effects of typical vs atypical?
- Typical - drowsiness, EPSE (severe), anticholinergic s/e (dry mouth etc), gynecomastia
- Dystonia
- Parkinsonian
- Akithisia
- Tardive dyskinesia (irreversible)
- Atypical - weight gain, metabolic syndrome, hyperglycemia
- General - both has EPSE (less in atypical), both give you reduction in cognitive function (mesocortical), both blunt mood (mesolimbic), risk of gynecomastia (tuberoinfundibular)
- Clozapine TRIAD - myocarditis, neutropenia, agranulocytosis
Brian Jones presents to the ED after a suspected stroke. On examination, his left eye is deviated down and out, his eyelid is slightly drooped and has paralysis of the right side of his body.
- Where do you suspect the lesion to be?
- What is the suspected artery involved?
- L) midbrain in the medial section (Left CN III palsy)
- PCA infarction ⇒ corticospinal tract (runs in medial section in midbrain) + CN III palsy
- Weber’s syndrome
Cerebral circulation supplies and findings if infarcted of:
Internal Carotid (ICA)
Cerebral circulation supplies and findings if infarcted of:
ACA
Cerebral circulation supplies and findings if infarcted of:
MCA
Cerebral circulation supplies and findings if infarcted of:
PCA
Cerebral circulation supplies and findings if infarcted of:
Lenticulostriate
Cerebral circulation supplies and findings if infarcted of:
ACA-MCA Watershed
Cerebral circulation supplies and findings if infarcted of:
MCA-PCA Watershed
BRAINSTEM circulation supplies and findings if infarcted of:
PICA
BRAINSTEM circulation supplies and findings if infarcted of:
PCA
BRAINSTEM circulation supplies and findings if infarcted of:
Basilar Artery
BRAINSTEM circulation supplies and findings if infarcted of:
AICA
BRAINSTEM circulation supplies and findings if infarcted of:
Vertebral + Spinal Arteries
BRAINSTEM circulation supplies and findings if infarcted of:
Superior Cerebellar Artery
Label the CN nerves
A 25-year-old woman presents with a third nerve palsy. Complete the following table:
Name the muscles of the eye
Review the action of each of these muscles from the neutral position.
IO = up & out
SO = down & out
SR = up /elevate
LR = abduct
MR = adduct
IR = down
Review the clinical testing used for the extra ocular eye muscles. Label the pictures below to indicate which extra ocular eye muscle would be isolated by each movement in both eyes for the H-test (i.e. not from neutral).
Follow the red arrows e.g. from eye pic middle left -→ SR would be needed to bring left eye up and IO will be needed to bring right eye up and a bit outwards
Explain the difference in clinical presentation between Horner’s Syndrome and a third nerve palsy
Review branches of external carotid
Seven Angry Ladies Fighting Over PMS
3 anterior, 1 medial, 2 posterior, 2 terminal
S - superior thyroid (anterior)
A - ascending pharyngeal (medial)
L - lingual (anterior)
F - facial (anterior)
O - occipital (posterior)
P - posterior auricular (posterior)
M - maxillary (terminal)
S - superficial temporal (terminal)
Review branches of internal carotid
Review Circle of Willis
It encircles/surrounds:
- Optic Chiasm
- Hypothalamus
- Midbrain
- Pituitary Gland
Review anterior and posterior blood supply to cerebrum
Compare and contrast the vascular territories of the four main sections of the MCA using the table below
Explain the difference between dysarthria, dysphagia and dysphasia. Provide an example of a neurological lesion (location and cause) that may result in the presentation of each of these symptoms.
Draw out the lateral and anterior corticospinal tracts on the template provided. Note the origin of each pathway, their decussation point and the muscles of the body that they innervate
A region of the temporal lobe has increased in size, compressing the surrounding structures.
The pupillary light reflex was performed on this patient and the results are presented below.
- Which nerve has been affected in the patient? Explain the rationale behind your answer.
- What nerves are involved in the pupillary light reflex? Draw out the pathway and explain why a direct and consensual pupil constriction can be elicited when light is directed into only one eye.
L) CN III damage ⇒ you don’t have direct response on L) eye, and no consensual on L) eye when light shone on R) eye
Afferent ⇒ CN II
Efferent ⇒ CN III
Light → retinal ganglion → optic disc → CN II (afferent) → optic chiasm → MGN → optic radiation → V1 (pretectal area) → edinger westphal (bilat) → CN III → ciliary ganglion → sphincter pupillae → pupillary constriction
You are reviewing the case of Alfred, a 76-year-old man, who has recently passed away.
An MRI taken in his recent history reveals the following:
- In which vascular territory does this tumor reside?
- Imagine you are performing a neurological examination on a patient with this tumor. What would you test and what would you expect to see from the examination?
- What side of the body would you expect to see any movement disorder? Explain your answer
PICA is the vascular territory
Tests:
- Gait - (heel to toe/figure of eight) - Ataxic
- Coordination
- Finger nose test - tremor on left side, past pointing/overshoot/undershoot
- Dysdiadochokinesis
- Balance problems
- Posture problem - wide-based stance, unsteady on their feet with eyes open.
What side of the body would you expect to see any movement disorder? Explain your answer
- Ipsilateral
- Left – left cerebellum connects with left side of the body – info has to go to the right primary motor cortex, then the corticospinal tract connects with the left side of the body
Briefly describe the general functions of each area (you don’t have to go into detail! Just demonstrate you understand the somatotopic arrangement of the cerebellum and understand the functions of the cerebellum).
Review Cerebellum anatomy and revise the blood supply to the cerebellum
Cytology reveals that the tumor in attached CT is the result of a metastasis. What is the most likely origin of this carcinoma? Where else might metastases be found?
- Melanocytes – derived from neural crest cells (PNS), closely related to neural tissue
- HER-2 positive breast cancers often metastasise to brain (pituitary)
- Renal, GI and pelvic cancers often metastasise to the brain
- This is a met melanoma: goes to liver, lungs, bone and brain (lung cancer was also reported MHx)
The following images reveal the morphology of the tumor. Describe what you can see from these images and what these images might tell you about the origin of the tumor.
The following images reveal the morphology of the tumor. Describe what you can see from these images and what these images might tell you about the origin of the tumor.
The following images reveal the morphology of the tumor. Describe what you can see from these images and what these images might tell you about the origin of the tumor.
Johnny was nauseous, vomited and reported having a headache. He subsequently lost consciousness.
- CT imaging was performed on Johnny. Based on his clinical presentation, which of the images below is most likely to represent the result observed for Johnny? Explain your reason by describing what you see in both images, with particular reference to the blood’s location with respect to the relevant meninges.
- Which type of vessel (arterial or venous) is likely to have been affected in Johnny’s case? Explain your answer based on Johnny’s clinical presentation. What vessels are associated with other meningeal bleeds?
What structures pass through the cavernous sinuses?
Content of cavernous sinus:
- CN 3, 4, V1, V2, 6
- Internal carotid
Whole L) face → LMN CN VII palsy (?bells)
How might you determine if other functions of the facial nerve have been affected?
- Loss of taste to anterior 2/3rd of tongue
- Hyperacusis (stapedius)
- Reduced lacrimation
- Reduced salivation
A colleague (not from UOW) believes that this must be CNV palsy, as this nerve also supplies muscles of the face.
Review the branches of the trigeminal nerve
- Ophthalmic
- Maxillary
- Mandibular
Explain the functions of the three branches of trigeminal nerve and compare/contrast these functions with those of the facial nerve.
Review the corticobulbar tract
Compare and contrast the clinical presentation of a lesion involving
i) optic nerve caused by MS,
ii) ischaemia of the optic tract.
Review the anatomical pathways involved in conjugate gaze and draw them below. Identify the nerves and revise their muscle innervation to enable conjugate gaze.
FEF → contralateral PPRF → interneuron to CN VI nucleus
- → MLF to contralateral CN III nucleus → medial rectus muscle of eyeball which is ipsilateral to FEF
- → CN VI nerve to Lateral rectus muscle of eyeball which is contralateral to FEF
NB: One and a half is damaged to PPRF + ipsilateral MLF to the PPRF and INO is damage to MLF only (can be unilateral or bilateral)
If i want to look to the right → activate L) FEF → decussates at PONS → R) PPRF → activated CN VI nuclei → R) eye looks right (LR activated) + activates contralateral MLF (left MLF) → L) CN III activated → L) MR muscle activated -> L) eye look right → conjugate gaze
Lola is a 67-year-old female, brought to ED following a motor vehicle accident. She was an unrestrained passenger in the vehicle during the head on collision and her head impacted the windshield. Neurological examination and investigations have determined that there has been a compression fracture resulting in both a paracentral and foraminal disc herniation.
- Draw a transverse plane cross-section of an intervertebral disc. Indicate the possible directions of disc herniations and the associated neural structures that would be affected.
Describe the anatomical location of the nerve root relative to the vertebral body within the cervical and lumbar spines.
Lola is a 67-year-old female, brought to ED following a motor vehicle accident. She was an unrestrained passenger in the vehicle during the head on collision and her head impacted the windshield. Neurological examination and investigations have determined that there has been a compression fracture resulting in both a paracentral and foraminal disc herniation.
Lola has Gr 1 power for shoulder abduction and Gr 3 elbow flexion. Ipsilateral Babinski’s signs are elicited. There is also inadequate respiratory effort, therefore she is placed on an artificial ventilator once stabilized.
- Identify the vertebral level where the compression has occurred (you can nominate two levels in your answer and be sure to include the IV disc level).
- Name the muscles involved in this assessment of this neurological upper limb presentation
- Review the CXR that was taken as part of the initial admission to hospital following the accident. What additional neurological injury is evident in the image?
- The patient returns for a follow up consultation 12 months following the accident. The doctor performs a neurological exam (power, sensation, reflexes). Name the four peripheral deep tendon reflexes within a neurological exam and name their spinal nerves involved in each reflex. State the expected outcomes of each reflex tested (i.e. a-reflexive, hypo or hyper-reflexive).
- The neurological exam finds that there is contralateral loss of nociception and temperature from the level of the injury and below. Which sensory pathway is affected?
- Identify the vertebral level where the compression has occurred (you can nominate two levels in your answer and be sure to include the IV disc level).
C4/C5 - shoulder abduction
- Involving C4 vertebral column
- C4 spinal nerve = above C4 bone, C5 nerve = below C4 bone
- Affecting spinal nerve C4-C5 & spinal cord at level of C4 vertebral body
- Name the muscles involved in this assessment of this neurological upper limb presentation
- C4 → traps & levator scap
- C5 → delt, Biceps brachii (musculocutaneous innervation → C5,6,7)
- Review the CXR that was taken as part of the initial admission to hospital following the accident. What additional neurological injury is evident in the image?
R) hemidiaphragm far lower → failure of respiratory effort → ?R) phrenic injury
The patient returns for a follow up consultation 12 months following the accident. The doctor performs a neurological exam (power, sensation, reflexes). Name the four peripheral deep tendon reflexes within a neurological exam and name their spinal nerves involved in each reflex. State the expected outcomes of each reflex tested (i.e. a-reflexive, hypo or hyper-reflexive).
UMN lesion C4
- S1 & 2 → achilles tendon → gastroc/soleus → hyperreflexive (UMN)
- L3 & 4 → patella tendon → quads → hyperreflexive (UMN)
- C 5,6 → Biceps tendon → hyporeflexive (LMN at C4-5 injury)
- C 7,8 → triceps tendon → hyperreflexive (UMN)
1,2 kick off your shoes → moving ankle → achilles
3,4 kick the ball → move knee → patella
5,6, pick up the stick → move forearm → biceps
7,8 shut the gate → external to internal rotation → triceps
- Which sensory pathway is affected?
Nociception & temp → STT (spinothal) → anterolateral
Review sensory pathways
Alex, a 50-year-old man, presents to the doctor with a friend who is concerned by his erratic behaviour. Alex’s friend notes that his personality seems to have changed over the past 9 months, and he has seemed to be very fidgety for a number of years, almost like he can’t sit still. In the past few weeks, there have been abrupt jerky movements that seem to affect his entire body.
- Compare and contrast the clinical presentation of Parkinson’s disease and Huntington’s disease. Which of these neurodegenerative disorders is Alex likely to be suffering from?
Review the anatomical structures that make up the basal ganglia. Using the coronal brain slice figure provided, map out the direct and indirect pathways of the basal ganglia.
Basal ganglia → subcortical nuclei responsible for motor control, motor learning, executive functions, behaviour, emotions.
Basal ganglia structures:
- Caudate nucleus
- Putamen
- Gpe & GPi
- Substantia nigra
- Subthalamic nucleus
Direct & Indirect pathway …..
Direct Pathway:
- SNpc produces Dopamine → activates D1 in striatum → causes production of GABA which inhibits GPi/SNr.
- GPi/SNr are inhibited from producing GABA so less inhibition of thalamus
- Reduced inhibition of thalamus = increased activity of thalamus to stimulate the motor cortex = movement
Indirect Pathway:
- ACH → increase in indirect pathway
- SNpc produces dopamine → binds to D2 receptor on Striatum and stimulates production of GABA which inhibits GPe
- Inhibition of GPe → reduced production of GABA to inhibit STN
- Reduced STN inhibition = increased production of glutamate by STN
- Increased glutamate by STN stimulates the GPi/SNr to produce +++ GABA that inhibits thalamus and subsequent stimulation of the motor movement → stops/slows movement
Identify the nuclei/neurons that degenerate in Huntington’s disease and explain how these cellular losses result in the clinical presentation.
Huntington’s → affects striatum → caudate nucleus + putamen (GPi+GPe)
- No caudate nucleus
- No GPi → less GABA produced → more movement → chorea
- No GPe → subthalamic nucleus receives a lot of inhibition by the initial indirect pathway → STN cannot produce glutamate & cannot stimulate SNr+GPi to produce GABA → there’s less GABA → thalamus no longer inhibited → increased movement → chorea
Jess’s ans (she said need more detail)
- Loss of D2 striatal neurons (part of the indirect pathway) and the aspiny cholinergic neurons in the striatum.
- Lose the ability to use the indirect pathway to reduce movement,
- Lose the ability of the cholinergic neurons to dampen the effects of the direct pathway
Review the structural relationship between nuclei of the basal ganglia, the internal capsule, the thalamus and the limbic system
Lola is a 67-year-old female, brought to ED following a motor vehicle accident. She was an unrestrained passenger in the vehicle during the head on collision and her head impacted the windshield. Neurological examination and investigations have determined that there has been a compression fracture resulting in both a paracentral and foraminal disc herniation.
Describe the clinical presentation of the spinal cord and/or peripheral nerve injury that would result from this trauma.
both a paracentral and foraminal disc herniation → direct n.pulposus leak to posterior segment of SC involving IVF ⇒ both central (same level of vert.column) & periprh (affect spinal nerve from the level above)
- Potential for both and both need to be assesses
- Paracentral– lose spinal nerve at affected area and cord tissue at that level
- foraminal disc herniation – spinal nerve
- Affected tracts – lose motor (CST) at and below the lesion
- UMN below the level → will shown hyper-reflexia etc (UMN clinical signs, babinski, disuse atrophy)
- LMN at the level (hypotonia, hyporeflexia)
- Because of injury at the SC level → impulse cant get through → LMN injury → eventually muscle atrophy (wasting atrophy)
- Will show LMN clinical signs (hyporeflex, hypotonia, fasciculation etc)
Q to jess ⇒
- If CST is damaged at level of lesion & below, why not sensory (DCML/STT)??
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