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Module 8: Neurosciences > PBL Learning Objectives > Flashcards

PBL Learning Objectives Flashcards

1
Q

Anatomy of the vertebral column, spinal cord and meninges (8.1)

A
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2
Q

Spinal tracts (ascending and descending) (8.1)

A
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3
Q

Causes of acute onset paralysis (8.1)

GBS, transverse myelitis, myasthenia gravis, polio, muscle diseases, botulism, ADEM, cord compression

A
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4
Q

Autonomic nervous system (arrangement, outflow and function) (8.1)

A

Sympathetic: Cells bodies within the lateral horns of levels T1-L2. Exit via the white ramus commicantes to enter the sympathetic chain. May synapse within the sympathetic chain or at distal ganglia.

Parasympathetic: Arises from cranial nerves (III, VII,IX and X) and S2-S4.

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5
Q

Causes of acute onset sensory loss (8.1)

A
  • Stroke
  • Spinal cord compression
  • Multiple Sclerosis
  • Diabetes Mellitus
  • Hypothyroidism
  • Vitamin B1, B6, B12 or E deficiency
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6
Q

Peripheral motor and sensory pathways (reflex circuits) (8.1)

A

Myotactic reflex - Knee jerk (muscle spindle)

Golgi tendon reflex

Flexor reflex

Crossed extension reflex

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7
Q

Anatomy of the meninges (8.2)

A

Extra dural space

Dura matter (periosteal and meningeal layers)

  • Reflections of the meningeal layer form the tentorium cerebelli, falx cerebri and falx cerebelli
  • The dural venous sinuses are formed by separations of the periosteal and meningeal layers - structure and names

Epidural space

Arachnoid matter

Subarachnoid space

Pia matter

Blood supply: Middle meningeal artery (from external carotid)

The Dura is innervated by branches of the trigeminal, glosspharyngeal and vagus nerves (V, IX and X). The high degree of overlap provides potential for referred pain.

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8
Q

Anatomy of the skull (8.2)

Bones of the skull, areas of importance, possible pathologies

A
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9
Q

Host response to infection (8.2)

A

The innate immune reponse initiates the sequence. The innate immuen system is non-adaptable and is ‘non-specific’ in its response (same response seen to multiple pathogens).

Recognition of foreign material through PAMP:PRR interactions.

Release of pro-inflammatory cytokines and complement induced inflammation.

Complement allows for opsonisation, neutralisation and/or cell lysis (via MAC).

Inflammation sees vasodilation (NO), increased vessel permeabilty (histamine) and formation of inflammatory exudate (rich in Igs and complement proteins).

Neutrophils are recruited to the site of damage/infection. Adhesion molecules (selectins, integrins etc) allow for extravasion.

Macrophages and leukocytes are later recruited - adaptive immunity.

Outcomes of inflammation include resolution, repair by fibrosis (loss of function), chronic inflammation (inflammation and repair occuring simultaneousy) and abscess formation.

T1 vs T2

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10
Q

Microbiology of meningitis and CNS infection (8.2)

A
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11
Q

Normal and abnormal CSF circulation (8.2)

A

Normal:

Lateral ventricles → cerebral aqueduct → third ventricle → intraventricular foramen → fourth ventricle → 2 x lateral and medial aperture → CSF enters the subarachnoid space → reabsorbed by arachnoid granulations → enters the dural venous sinus

Abnormal CSF circulation - Hydrocephalus: Increased CSF volume, dilation of the ventricles +/- raised intracranial pressure

Communication hydrocephalus: Decreased CSF absorption by arachnoid granulations. Increased ICP, papilloedema and herniation

Normal pressure hydrocephalus: Idiopathic, seen in the elderly. Dispansion of the ventricles disrupts the corona radiata leading to ‘wet, wobbly and wacky’ symptoms (incontinence, ataxia and cognitive dysfunction)

Non-communicating (obstructive) hydrocephalus: Structural blockage of the ventricles (e.g. colloid cyst)

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12
Q

Meningitis vaccination programme (8.2)

A

Meningitis B Vaccine

6-in-1 vaccine: Protects against Haemophilus influenzae type B (Hib), an organism that can cause meningitis

Pneumococcal vaccine: Protects against meningitis

Hib/Men C vaccine

MMR vaccine: Meningitis often occurs as a complication of these conditions

Meningitis ACWY vaccine: Protects against meningococcal groups A, C, W and Y which cause meningitis

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13
Q

Symptoms and sign of meningitis (8.2)

A

Signs and symptoms of bacterial meningitis:

  • Fever
  • Severe headache
  • Neck stiffness
  • Photophobia
  • Altered mental state
  • Vomiting seizures
  • Nuchal rigidity: A stiff neck with resistance to passive flexion
  • Rash: Primarily associated with meningococcal meningitis
  • Signs of raised ICP: Papilloedema, bulging fontanelle
  • Evidence of a primary source of infection: Pt may have had sinusitis, pneumonia, otitis media or mastoiditis
  • Positive Kernig’s and Brudzinski’s signs

Viral meningitis signs and symptoms

  • Often self-limiting with no serious sequelae
  • Similar presentation to bacterial meningitis
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14
Q

Antimicrobrial treatment of bacterial meningitis (8.2)

A

If identified in the community, prior to transfer to hospital administer benzylpenicillin.

> 1 month, < 50 years of age

1st line: Dual antibiotic therapy of vancomycin + ceftriaxone/cefotaxime

Adjunct: Supplemental oxygen

Adjunct: Dexomethasone - Reduces rates of hearing loss and neurological sequelae

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15
Q

Lumbar puncture - indications and contraindications (8.2)

A

Indications: Suspected CNS infection e.g. meningitis, encephalitis (presents with altered mental state), suspected subarachnoid haemorrhage

Contraindications: Unresolved coagulopathy, signs of raised ICP (papilloedema, bulging fontanelle, drowsiness, diplopia), infection at the LP site

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16
Q

Immunological conditions pre-disposing to infection (8.2)

A
  • HIV
  • SKID
  • Transplantation
  • Immunosuppressive therapy e.g. systemic corticosteroids
  • Thymus disorder
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17
Q

Long term sequelae following meningitis (8.2)

A
  • Cognitive, behavioural and academic problems
  • Hearing loss (sensorineural - 25 - 35 % of pts following pneumococcal meningitis)
  • Seizures

Complications include: Shock, coagulopathy, endocarditis and pyogenic arthritis

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18
Q

Management of sepsis and meningitis (8.2)

A
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19
Q

Altered consciousness and epilepsy (8.3)

A
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20
Q

Cortical localisation of function (8.3)

(Brodmann’s areas and homunculus)

A
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21
Q

Risk factors for TIA and stroke (8.3)

A

Hypertension

Age ( > 55)

Diabetes

Atrial fibrillation (formation of emboli)

High cholesterol levels

Obesity

FHx

Increased oestrogen levels (oestrogen promotes coagulation)

Smoking

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22
Q

Aetiology of epilepsy (8.3)

A

Epilepsy describes an increased propensity for the hypersynchronus discharge of seizures, leading to seizures.

Epilepsy may be resultant of structural malformations (tumours, scars) or may be congenital (channelopathies, abnormal cortical neural networks).

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23
Q

Differential signs of epilepsy, stroke and psychiatric disease (8.3)

A
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24
Q

Classification of seizures (8.3)

A
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25
Q

Space occupying lesions (8.3)

Consequences

A

Tumours (primary or secondary/metastatic)

Vasculature: Haematoma, aneurysms, stroke & TIAs,

Inflammatory: Abscesses, tuberculoma

Parasitic

Consequences:

  • All cause intracranial pressure to increase
  • The cranial tissue (cerebrum and ventricles) becomes distorted and displaced by the lesion
  • The function of the neural tissue is disrupted and seizure activity may result
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26
Q

Usefulness of tests in diagnosing epilepsy (8.3)

A
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27
Q

Anti-epilepsy drugs (8.3)

A

Sodium valporate: Inhibits the metabolism of GABA; inhibits Na+ and Ca2+ channels. Potentiates the inhibitory effects of GABA

Carbamazepine: Inhibits Na+ channels

Lamotrigine: Inhibits Na+ channels

Phenytoin: Inhibits Na+ channels

Gabapentin: Inhibits Ca2+ channels

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28
Q

Effects of anti-epileptic drugs on foetal development (8.3)

A

Can greatly increase the risk of foetal congenital malformations.

Sodium valporate:

Spina bifida, atrial septal defect, cleft palate, hypospadias

Increased risk of autism spectrum disorder and long-term developmental disorders

Carbamazepine:

Defects in the neural tube, urinary tract, CV system and cleft palate

Phenytoin:

Cleft palate

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29
Q

Brain tumours: Types, progression, prognosis (8.3)

A
30
Q

Diagnosis of epilepsy and road traffic regulations (8.3)

A

Diagnosis of epilepsy must follow 2 or more unprovoked seizures in a period of less than 24 hours.

Road traffic regulations:

If an individual has had 1 or more seizures then certain medical standards must be met to allow them to drive.

Group 1 licenses: Completely free of seizures for 1 year, with or without taking anti-epileptic medications

Group 2 licenses: Must have been seizure free for 10 years, with or without taking anti-epileptic medications

31
Q

Management of epilepsy (8.3)

A

Medication

VNS (vagal nerve stimulation)

Ketogenic diet

32
Q

Assessment of suicide risk (8.4)

A

Tool for assessment of suicide risk - TASR

Key risk factors:

  • Previous suicide attempt
  • Current suicide plan
  • Access to lethal means
  • Hx of psychiatric disorder
  • FHx of psychiatric disorder or suicide
33
Q

Causes of facial pain, including dental and gum pathology (8.4)

A
  • Tempromandibular joint (TMJ)
  • Dental: Dry socket (following wisdom tooth removal); neurological
  • Salivary gland disorders: Sialolithiasis (usually within the submandibular gland)
  • Air sinuses: Sinusitis
  • Migraine: May be bi- or unilateral
  • Cluster headache: Quick onset with unilateral intense pain, often around the eye, temple and sometimes face
  • Trigeminal neuralgia: Unilateral sharp, ‘electric shock’ like pain experienced. Unremarkable findings in other areas of examination.
  • Gingivitis
  • Tumour (secondary)
  • Giant cell arteritis: A granulomatous vasculitis that commonly affects branches of the external carotid artery. DO NOT MISS as may cause unreversible blindness due to optic nerve ischaemia. Headache, visual disturbances and jaw claudication
34
Q

Cranial nerves V and VII (8.4)

A
35
Q

Depression: Diagnosis and management (8.4)

A

Diagnosis:

  • Symptoms: Patients may present with a history of depressed, anxious, irritable, or flat mood, anhedonia, weight changes, libido changes, sleep disturbance, psychomotor problems, low energy, excessive guilt, poor concentration, or suicidal ideation.
  • Verbal screening questions may be used to indicate whether a more extensive screening questionaire is required
  • PHQ-9 (Patient Health Questionaire)
  • HADS (Hospital Anxiety and Depression Scale)
  • Testing may be carried out to exclude other conditions which may stimulate these symptoms e.g. hypothyroidism, Cushing’s, B12 deficiency

Management

  • CBT, psychotherapy
  • SSRIs, SNRIs, TCAs
  • Referral to crisis team?
  • ECT (elevates serotonin and NA levels via inducing seizure activity)
36
Q

Sensory and motor innervation of the face (8.4)

A

Muscles of mastification: Mandibular branch of the trigeminal nerve (Vc)

  • Temporalis, masseter, lateral and medial pterygoid, mylohyoid, anterior belly of digastric

Muscles of facial expression: Terminal branches of the facial nerve

  • Orbicularis oculi, orbicularis ori, buccinator. platysma

Sensory innervation: Branches of the trigeminal nerve

37
Q

CBT and non-pharmological therapies for depression (8.4)

A

CBT:

  • Helps management of problems by changing ways of thinking and behaviour
  • Deals with current problems
  • Develops strategies for responding to situations, should they arise again

ECT:

  • Whilst under general anaesthetic an electrical current is passed through the brain, prompting seizure activity
38
Q

MOA of antidepressants (8.4)

A

Act to increase levels of monoamines - specifically serotonin and noradrenaline. Act through inhibition of reuptake receptors (SERT or NET) or through modulating metabolism of the neurotransmitter (MAOIs)

39
Q

Neuropharmacology of depression (8.4)

A

Increased activity within the frontal lobe whilst activity is decreased within the limbic system. Pre-frontal cortex, amygdala and hippocampus are implicated. Abnormal levels of certain hormones, elevated CRH and cortisol, hence the hypothalamus may be implicated.

40
Q

Treatment of neuropathic pain (8.4)

A

Neuropathic pain: Severe, chronic pain resultant of neurological conditions affecting the sensory pathway, that is unrelated to peripheral tissue injury. Related to the redistribution of Na+ channels and the appearance of alpha adrenoreceptors, allowing for sympathetic medited pain.

Treatment:

  • Opioids (?) - although can be termed ‘opioid resistant’
  • TCAs: E.g. amitriptyline
  • Gabapentin: Act by inhibiting the α2δ subunit of Ca2+ channels - preventing NT release, which is upregulated on damaged sensory neurons
  • Carbamazepine: Blocks Na+ channels. Effective for trigeminal neuralgia
  • Other anticonvulsants, such as valporate and lamotrigine, can be effective
  • Lidocaine: Local anaesthetic drug used topically. Blocks spontaneous discharges from damaged sensory terminals
41
Q

Outline the stages of bereavement (8.4)

  • Kubler-Ross grief cycle
  • TEAR model
A
42
Q

Blood supply to the brainstem and cerebellum (8.5)

A
43
Q

Blood supply to the forebrain (8.5)

A

Anterior cerebral artery - Anteromedial aspect of the brain

  • Branch of the ICA

Middle cerebral artery - Lateral aspect of the brain

  • Branch of the ICA
44
Q

Production of speech (8.5)

A

The intrinsic muscles of the larynx are responsible for the production of speech through control of the rima glottis and the vocal folds.

Innervation: SCAR

Superior laryngeal nerve( CN V) - cricothyroid all others = recurrent laryngeal (CN V)

Posterior cricoarytenoid muscle is the only abductor of the vocal folds.

* Extrinsic muscles of the larynx are responsible for depression and elevation of the larynx

45
Q

Risk factors for stroke (8.5)

A
  • Age
  • Smoking
  • Hypertension
  • Diabetes
  • AF
  • Hx of liver failure (decreased production of clotting factors)
  • Internal carotid artery stenosis
46
Q

Causes of stroke (8.5)

A
47
Q

Pathophysiology of cerebral ischaemia/infarction (8.5)

A

Ischaemic:

  • Occlusion of vessels interrupts blood supply to the cerebrum, arterial branch points are particularly affected
  • The area becomes deprived of oxygen, preventing synthesis of ATP and therefore depriving neuronal cells of energy
  • The cell undergo necrosis, specifically liquefactive
  • Neurological deficit results

Haemorrhagic (intracerebral or sub-arachnoid):

  • Rupture of the vessel causes release of blood
  • Nearby structures become compressed, leading to neurological deficit
48
Q

Differences between dysarthria and aphasia (8.5)

A
49
Q

Functional anatomy of cranial nerves IX, X and XI (8.5)

A
50
Q

Functional anatomy of speech and swallowing (8.5)

A
51
Q

Innervation pattern for facial nerve LMNs (8.5)

A
52
Q

Clinical classification of strokes (8.5)

A

OCSP/Bamford classification

TACS - Total anterior circulation stroke. Poor prognosis

PACS - Partial anterior circulation stroke. Good chance of recovery

POCS - Posterior circulation syndrome. Most common, good prognosis

LACS - Lacunar circulation syndrome. Good recovery

Anterior circulation: ACA and/or MCA

Posterior circulation: PCA

53
Q

Investigation of the stroke patient (8.5)

A

CT scan - Allows differentiation of ischaemic/haemorrhagic stroke

FBC - Rule out anaemia, thrombocytopenia as possible causes

Blood glucose - To rule out hypoglycaemia as a possible cause

Hyperglycaemia → worse prognosis

U&E - Rule out electrolyte imbalance as a possible cause

ECG - Check for any CV manifectations/complications

Lipid profile - Check for hyperlipidaemia, possible role in pathology

INR/PTT - Check for hypocoaguable state, > chance of bleed (may require correction)

54
Q

Neuroprotection agents in stoke (8.5)

A

NMDA antagonist:

  • Prevents glutamate from binding, and subsequently activating, the receptor

Nalmefene - narcotic receptor antagonist:

  • Reduces the levels of excitatory neurotransmitters contributing to cellular injury in early ischaemia

Lubeluzole

  • MOA unclear - may block Na+ channels, reduces NO release

Target free radical generation

Monoclonal antibodies to block ICAM

  • Decreases reprofusion injury
55
Q

Parkinson Disease (8.6)

A
56
Q

Balance and its control (8.6)

A

Maintenace of balance is dependent upon 3 factors:

  • Vision
  • Proprioception (DCML pathway)
  • Vestibular system (15 %) (vestibulospinal tract)

Loss of one of these inputs can be compensated for by the other inputs. However, loss of 2 inputs leads to problems with balance.

57
Q

Basal ganglia, internal capsule and limbic system (8.6)

A
58
Q

Initiation, execution, coordination and control of movement (i.e. The motor system and its components) (8.6)

A
59
Q

Neurotransmitters in the motor system (8.6)

A

Dopamine - Promotes movement

Glutmate - Promotes movement

GABA - Inhibits movement

60
Q

The pyramidal and extrapyramidal tracts (8.6)

A
61
Q

State key signs of raised intracranial pressure and possible causes (8.2)

A
  • *Nausea/vomiting
  • Visual disturbance
  • *Headache
  • *Papilloedema
  • Confusion
  • Loss of pupillary light reflex

Causes of raised intracranial pressure:

Localised mass lesions, CSF circulation disruption, disruption to dural venous sinus circulation, diffuse brain oedema/swelling

62
Q

Function of myelin (8.7)

A

Formed by oligodendrocytes in the CNS (1 cell in contact with multiple neurones) and Schwann cells in the PNS

The myelin acts to increase the speed/velocity of electrical conductance along the axons of neurones.

Myelinated areas of the action see less leakage of ions. Ion channels are concentrated at unmyelinated regions.

Action potentials travel between the nodes of Ranvier via saltatory conduction.

> axonal diameter also increases conduction velocity - allows for decreased ionic resistance.

63
Q

Incontinence (8.7)

Review micturition

A
64
Q

Pathogenesis of multiple sclerosis (8.7)

*Keywords*

A

A T cell mediated autoimmune disease that causes an inflammatory process in the white matter of the CNS.

Activated T cells seek entry into the CNS, breaching the BBB. This causes upregulation of adhesion factors and further influx of inflammatory cells. The release of cytokines from T cells causes direct toxicity and attracts macrophages, which contribute to demyelination. This leads to the formation of plaques/sclera. In the early stages of the disease remyelination may be seen but as oligodendrocytes suffer more damage this is prevented.

Epitope spread occurs early on.

Demyelination disrupts axonal support and leads to the destabilisation of axonal membrane potentials.

Multifocal areas of demyelination result

65
Q

Rehabilitation/community support of MS (8.7)

A
66
Q

Visual pathways, reflexes and eye movements (8.7)

A

Review:

  • Optic pathway
  • Pupillary light reflex
  • Accomodation reflex
  • Movements and innervation of the rectus and oblique muscles
67
Q

Prognosis of multiple sclerosis (8.7)

A
68
Q

Treatments for multiple sclerosis (8.7)

A

Stop relapses and modify progression with disease modifying therapies: beta-interferon; natalizumab (reduced WBC adhesion and migration)

Treatment of acute flares: Corticosteroids

Symptomatic relief:

  • Neurogenic bladder: Catheter, M3 antagonists
  • Spasticity: Baclofen, GABA receptor agonists
  • Pains: TCAs, anticolvulsants
69
Q

Types of multiple sclerosis (8.7)

A

Relapsing-remitting

Primary progressive

Secondary progressive

70
Q
A

Module 8: Neurosciences (19 decks)

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