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Neuroscience 2020 > Pathophysiology & details of neurological conditions > Flashcards

Pathophysiology & details of neurological conditions Flashcards

1
Q

What are Peripheral Nerve injuries?

A

When compression, traction or transection interrupts peripheral nerves it leads to a peripheral nerve disorder.
This results in ipsilateral motor & sensory impairments usually restricted to a specific body segment.

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2
Q

What is an ABI?

A

An Acquired brain injury is one that occurs after birth. E.g. a traumatic brain injury (TBI)

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3
Q

What is a TBI?

A
  • CNS disorder, an ABI caused by a traumatic event.
  • One or more structure is affected – widespread & multifocal/ diffuse compromise
    1. Rapidly moving hard object hits a stationary head
    2. Rapidly moving head hits a stationary hard surface
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4
Q

TBI diagnosis?

A 
Clinical assessment as well as scan evident (CT, MRI)
PTA test (post-traumatic amnesia)
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5
Q

TBI Classification?

A

Subdural Haematoma: Venous bleed below the dura

Epidural Haematoma: Arterial bleed between skull & meninges into extradural space - causes pressure on brain & compromise of tissue

Diffuse Axonal Injury – Sheer and stretch injury to neurons that have long axons travelling up and down from the brain

Intracranial haemorrhage – Haemorrhage/ bleeds within brain tissue

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6
Q

TBI problems?

A
  • S, M & or C/P
  • Typical issues with cognitive circuits: Problems with the frontal lobe/ pre-frontal (also cerebellum & BG)
    1. Level of consciousness
    2. Attention, insight, memory, emotion, intellectual function
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7
Q

TBI management?

A

CONSERVATIVE: Monitoring of Intracranial Pressure (ICP)

SURGICAL: Piece of skull removed to get to brain tissue:

  • Craniectomy: bone left out, to remove swelling or bleeding, recover space
  • Craniotomy: bone replaced within the same surgery
  • Extra Ventricular Drain (EVD): drain fluid & keep ICP normal
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8
Q

What is a Stroke?

A

A blockage (ischemic) or rupture (haemorrhagic) to blood vessels in the brain, causing a loss of blood supply to regions of the CNS and therefore sensory, motor &/or cognitive & perceptual impairments lasting over 24 hours (under 24 hrs = transient ischaemic attack).

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9
Q

What are the types of Ischaemic stroke?

A

Embolic - blockages of a blood vessel supplying neural tissue, caused by a blood clot that has developed & travelled from another area of the body.
Thrombotic - blockages caused by development of plaques in blood vessels supplying neural tissues.

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10
Q

What are the types of haemorrhagic strokes?

A

Intracerebral - ruptured blood vessel resulting in leakage of blood into the brain tissue.
Intracranial - ruptured blood vessel resulting in leakage of blood between the skull & meninges that cover the brain.

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11
Q

How is a stroke diagnosed?

A

Clinical assessments & evidence of injury on scans.

  • Pre-frontal cortex & posterior parietal cortex - cognitive & perceptual impairments
  • Primary motor cortex (back of frontal lobe) - motor impairments
  • Primary somatosensory cortex - SS impairments
  • Primary visual cortex (occipital lobe) - visual impairments
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12
Q

What are the 4 sub-classifications of strokes using the oxford/Bamford classification system?

A

TACS - Total Anterior Circulation stroke
PACS - Partial Anterior Circulation stroke
POCS - Posterior Circulation stroke
LACS - Lacunar stroke

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13
Q

What are TACS & PACS strokes caused by?

A

Compromised integrity of the anterior circulation of the brain. Mainly the Anterior cerebral artery (ACA) & Middle cerebral artery (MCA) that supply the frontal & parietal lobe.

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14
Q

What typical problems present in patients with TACS & PACS strokes?

A

S, M &/or C/P impairments. TACS must have 3 & PACS 2 of the following three problems:

  1. Hemiparesis &/or hemisensory loss (face, trunk, limbs)
  2. Homonymous hemianopia
  3. Cognitive/ perceptual
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15
Q

What are POCS strokes caused by?

A

Compromised integrity of the posterior circulation of the brain, cerebellum &/or brainstem. Mainly the posterior cerebral artery (PCA), basilar artery & vertebral artery.

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16
Q

What typical problems present in patients with POCS strokes?

A

S, M, &/ or C/P impairments. POCS stroke patients need 1 of the following problems:

  1. Homonymous hemianopia
  2. Cerebellar impairments, vestibular impairments
  3. Cranial nerve impairments - brainstem compromise
  4. Sensory &/ or motor impairments
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17
Q

What are Lacunar strokes caused by (LACS)?

A

Lacunar strokes are caused by compromised integrity of the smaller blood vessels that have branched off of the ACA & MCA supplying deep structures of the brain.

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18
Q

What typical problems present in patients with LACS strokes?

A

S & M impairments. Patients need 1 or more of these problems:

  1. somatosensory
  2. motor
  3. somatosensory & motor
  4. ataxic hemiparesis
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19
Q

Typical surgical vs conservative management of Ischaemic strokes?

A

Surgical - Endovascular clot retrieval (tube fed through a blood vessel to remove the blood clot)
Medical -Thrombolysis (administration of a drug – breaks down clot)

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20
Q

Typical surgical vs conservative management of haemorrhagic strokes?

A

Surgical - repair rupture

Medical - drugs to reduce BP, counteract blood-thinning agent, slow down bleeding

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21
Q

What is Parkinson’s disease?

A
  • A neurodegenerative, hypokinetic disorder affecting the Basal Ganglia + other substructures
  • Usually diagnosed in older adulthood & more in Males > females
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22
Q

Whats is a HYPOKINETIC disorder?

A

A CNS disorder causing less movement than normal, slower & smaller. E.g. Parkinson’s disease

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23
Q

Explain the Pathophysiology of Parkinsons disease?

A
  1. The cerebral cortex delivers a plan for movement to basil ganglia for review & processing
  2. The basal ganglia consist of nuclei - they work together to process motor plan
  3. Plan sent to the thalamus (relay centre of the brain) -then back to the cerebral cortex
  4. ## CC executes the plan by a UMN in the corticospinal tract = which results in movement
  5. A Lack of dopamine production in substantia nigra disrupts the function of basal ganglia (& frontal lobe).
  6. This Excessively inhibits the cortex from eliciting movement
  7. This Abnormally functioning BG means that overall output to CC is less than normal and therefore movement extremely slow & small
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24
Q

What are the typical impairments seen in a patient with Parkinson’s disease?

A

M & C. Patient needs 2 of 3 cardinal signs:

  1. Bradykinesia
  2. Rigidity
  3. Resting Tremor
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25
Q

What is Bradykinesia?

A

Slower than normal movement

Seen in Parkinsons disease.

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26
Q

What is Rigidity?

A

Abnormal muscle tone causing hypertonia - not velocity dependent.
Seen in Parkinsons disease.

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27
Q

What is a Resting Tremor?

A

Involuntary movements/ tremors.

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28
Q

Explain the medical management for Parkinsons disease?

A

Replacement of dopamine.

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29
Q

How do you classify the stages of Parkinsons?

A

Hoehn & Yahr Stages: 1-5 - Further up the scale, the less function

30
Q

What is a SCI?

A

A spinal cord injury is a CNS disorder characterised by compromised integrity of the spinal cord.
The level of the injury can vary - Cx, Tx, Lx
Extent of the injury can vary - complete vs incomplete

31
Q

Explain the pathophysiology of a SCI?

A

Can have atraumatic (stroke, degeneration of SC, MS, Cancer, infection) or traumatic (MVA, falls ect.) causes

32
Q

How do you diagnose a patient with a SCI?

A

Clinical assessment & scans.

Diagnostic outcome measure: Pinprick – ventral, Light touch - dorsal, Corticospinal pathway: 5 muscle groups

33
Q

What are the classifications of a SCI?

A
  • Neurological Level: Level of the spinal cord with normal sensory and motor function bilaterally e.g. C7 - All levels above normal sensory and motor function
  • Severity of Injury at the Level: A–E, A (complete lesion - no function below VS further up the scale - the more function you have, B, C, D incompletes, E = normal function
  • Tetraplegia / Quadriplegia: People with Cervical SC Injury – affecting all limbs and trunk
  • Paraplegia (lower limbs & trunk): Thoracic SCI – trunk & lower limbs
  • Lumbar & Sacral SCI - lower limbs
34
Q

Typical problems that present in patients with a SCI?

A

Bilateral S M impairments. Motor = weakness & abnormal muscle tone
- hypertonia (too much tone & is resistant to stretch) - leads to velocity-dependent spasticity

35
Q

Explain the pathophysiology of a cauda equina injury & the common impairments?

A

Compromised integrity of the cauda integrity (PNS disorder)
The level of injury can vary - the extent of the injury at the level can vary (complete vs incomplete).
The cause can be traumatic or atraumatic.
Bilateral S & SS
Bilateral paresis & hypotonia

36
Q

What is MS?

A
  • Multiple sclerosis is a demyelinating disease confined to CNS.
  • Autoimmune, Degenerative & Progressive neurological condition
  • Onset young adulthood, Females > males
37
Q

What is BPPV?

A

Benign Paroxysmal Positional Vertigo. It is a Mechanical vestibular health condition in the PNS (most common vestibular disorder).

38
Q

Explain the pathophysiology & aetiology of BPPV?

A
  • BPPV is caused by the displacement of otoconia into Semicircular Canal (SC) (normally in utricle and saccule)
  • Posterior SC most commonly affected (PC-BPPV)
  • Prevalence increase with age > 65 yo
  • Trauma (i.e. head injury)
  • Vestibular Neuritis (more than one category)
39
Q

What are the two types of visual impairments?

A

Visual field loss: dysfunction of the sensory pathway from the eye to the brain.
Double vision: dysfunction of the motor system that controls eye movement from the brainstem to the eye.

40
Q

Explain the two types of visual field loss.

A

Monocular visual loss - damage to CNVII before the optic chiasm. Lose vision from one whole eye.
Homonymous Hemianopia - damage to CNVII after the optic chiasm. Loss of one visual field (either L or R) brom BOTH eyes.

41
Q

Explain the cause of double vision, how does this differ from normal vision?

A
  • Caused by the weakness of muscles innervated by CN VII, IV, VI, or the connections between their nuclei in the - brainstem, OR cerebellum & CC
  • Causing the eyes to not move together
  • Meaning one eye is looking in one direction and the other eye is looking in the other direction so that the brain receives images of two different objects at the same time from the two eyes looking in different directions.
  • In the normal binocular vision, the eyes are positioned such that the fixated image falls in exactly the same spot on the retina of each eye - therefore the brain receives the same image from both eyes
42
Q

Explain the NORMAL function of the Vestibular system.

A
  • Its job is to Detect position & movement of the head e.g rotation L & R.
  • This system is constantly active, even at rest (~ 100 spikes/ APs per sec) “tonic firing”
  • Movement of head – modulate firing rate on both sides
  • Rotating head to the L - Increased firing rate on L & decreased firing rate on R
  • Change in firing rate normally equal in magnitude, opposite in direction
  • CNS receives information from both sides of the PNS & interprets equal & opposite changes in firing rates from either side of PNS to identify head movement
43
Q

Explain the ABNORMAL function of the vestibular system.

A
  • At rest: the CNS is receiving different firing rates from the L & R PNS sides. If the input received from both sides isn’t equal at rest – then the vestibular system interprets this as movement.
  • With movement: information delivered is not equal & opposite.
44
Q

List typical vestibular impairments.

A
  • Vertigo (dizziness, the environment is moving)
  • Nystagmus (abnormal eye mvt)
  • Postural Instability (balance)
  • Nausea
  • Vomiting
45
Q

What is vertigo?

A
  • Vestibular impairment
  • Movement of the environment that isn’t actually occurring
  • Typically experience nystagmus at the same time
  • If it doesn’t sound like vertigo, check for other causes of dizziness (e.g. cardiovascular)
46
Q

What is nystagmus?

A
  • vestibular impairment
  • Eye movement (Fast in one direction, Slow in the other)
  • Direction of the nystagmus is named after the fast component (R/L)
  • Can be horizontal (PNS), vertical (CNS) and torsional
  • Normal (end range physiological nystagmus), Abnormal (at or within 30° from midline)
47
Q

What is vestibular neuritis?

A
  • Peripheral acute vestibular syndrome
  • Inflammation of the vestibular division of CNVIII Vestibular nerve)
  • Most often on one side only (left or right) – unilateral - - - - Usually caused by a virus
48
Q

What are the two categories of vestibular health conditions?

A

BPPV and Acute Vestibular Syndrome (peripheral or central)

49
Q

What are the conditions that fall under the categories of Peripheral & Central acute vestibular syndromes?

A

Peripheral: Vestibular neuritis
Central: Stroke, TBI, MS, Tumour

50
Q

What should you ask during the subjective assessment with someone you suspect has a vestibular dysfunction?

A
  1. Describe their dizziness (- the term dizzy)
  2. Describe episodes of dizziness (+++ 1st & most recent episode)
  3. Duration of dizziness - the time is critical to establish – less (BPPV) or more than 1 minute
51
Q

What should you look for during an objective assessment of someone you suspect has a vestibular dysfunction?

A
  • Eyes: look for nystagmus: assess CNVIII - 1st spontaneous & 2nd gaze evoked (T & X test)
  • Cervical ROM (screen for HIT)
  • Head Impulse Test (HIT) – vestibulo–occular reflex (normal or abnormal)
  • Vertebral Basilar Artery Insufficiency Test (VBI)
  • Dix-Hallpike Test (BPPV – PC)
  • Balance: Clinical Test Sensory Interaction in Balance (CTSIB); Fukuda
52
Q

Explain the difference between a UMN lesion and a LMN lesion in the spinal cord.

A

C6 level compromise/ lesion for example – means UMN lesions to all UMNs descending through that segment. Everything from C7 & below UMN will be compromised leading to Hypertonia (spasticity (LMN are preserved))
At the C6 - LMN synapsing at this level will also be compromised therefore Hypotonic muscle tone occurs (UMN & LMN are compromised)

53
Q

Explain the pathophysiology of multiple sclerosis:

A
  • Destruction of the myelin covering the axons of neurons in the CNS by the immune system (abnormal immune response) .
  • This compromises nerve conduction resulting in a reduced speed of nerve conduction or Absent nerve conduction (can’t propagate action potential)
  • Leading to either reduced or absent function in the individual
  • Multiple areas of CNS affected by the development of sclerotic plaques because of the destruction of myelin
  • Relapses happen but myelination can occur (recover function)
  • Axons can also get damaged in this process
  • Inflammatory process – the breakdown of myelin - sclerotic plaques/ scar tissue forms
54
Q

How do you diagnose MS?

A
  • You need clinical evidence of 2 episodes (attacks) of neurological dysfunction
  • e.g. reports loss of vision from one eye (very blurry for a few days and resolved, three months later: weakness and tingling in both legs - this gives evidence of lesions
  • MRI – Visual evidence of multiple lesions in diff areas of the CNS
  • Lumbar puncture
55
Q

Typical impairments in a patient with MS?

A
  • Demyelination can occur anywhere in the white matter of the CNS = variable impairments: S, M,C/P
  • Common initial problems: S(Vi)
  1. Loss of vision in one eye (visual field, acuity): CNII (Optic)
  2. Diplopia: weakness in extraocular eye muscles from lesions to circuitry within CNS that innervates CNIII, IV, VI
  • Areas of white matter (myelinated): Cerebral Hemispheres, Brainstem, Cerebellum, Spinal Cord, Optic Nerve
56
Q

Classifications of MS?

A

Benign: 1 or 2 relapses, full recovery & no long-term disability
Relapsing Remitting: Series of relapses/ attacks, partial or complete recovery after emissions, loss of function/ gain of function
Secondary Progressive: Subtype occurring after initially presenting as relapsing remitting,
Primary Progressive: Continuous loss of function from onset

57
Q

What impairments occur in an MS patient with a cerebellar lesion?

A
  • Damage unilateral = symptoms appear on the side of the lesion (ipsilateral (L- L))
  • Cognitive affective syndrome occurs following cerebellar damage (emotional)
  • Primary afferent neurons originating in the vestibular apparatus enter the brainstem, some terminate in the vestibular nucleus, some terminate in the cerebellum

Motor:

  • Abnormal muscle tone (hypotonia)
  • Coordination: Ataxia, Intention Tremor, Dysmetria, Dysdiadochokinesia: can’t perform rapidly alternating mvts, Dysarthria: uncoordinated speech, slurred

Sensory (Ve):

  • Vertigo>1minute
  • Nystagmus
  • Nausea
  • Vomiting
  • Balance

Cognitive

  • Affective problems
  • Disinhibition
  • Inappropriate behaviour
  • Planning & memory
58
Q

Define a Peripheral Nerve Injury (PNI): Which neurons are compromised & what impairments are seen?

A
  • A PNS disorder caused by the Interruption of peripheral nerve(s) by Compression, traction, transection
  • LOWER MOTOR NEURONS are compromised
  • IPSILATERAL SENSORY AND MOTOR IMPAIRMENTS
  • Typically restricted to a body segment (i.e. upper or lower limb)
  • Paresis, SS issues & HYPOTONIA
59
Q

Define Huntington’s disease

A
  • RARE CNS disorder (basal ganglia & other structures) – similar to PD
  • genetic - inherited from a parent
  • Neurogenerative disorder (10-20 years till death)
  • HYPERKINTIC disorder
  • Typically diagnosed in younger adulthood, males >females
60
Q

Explain the Pathophysiology of HD?

A
  • Atrophy of striatum – caudate nucleus & putamen
  • Glutamate toxicity affecting the Indirect mvt pathway:
    1. Glutamate released in stratum by cortical neurons – excitotoxicity (too much glutamate)
    2. Death of neurons originating in striatum = atrophy
    3. Striatum neurons can’t inhibit STN neurons
    4. STN neurons inhibit STN neurons
    5. STN neurons can’t excite GPi/SNpr neurons
    6. GPi/SNpr can’t inhibit thalamus = HYPERKINESIA
61
Q

What common impairments are seen in a patient with Huntington’s disease?

A 
Motor impairments: 
Hyperkinesia - Chorea/ choric movement
-	Involuntary mvt
-	Jerky mvt 
-	Abnormal muscle tone – hypotonia 
Cognitive/ perceptual impairments
62
Q

What is Cerebral Palsy?

A
  • CP is a group of heterogeneous neurological disorder resulting in impairment of mvt, muscle tone, posture. & comorbidities e.g. pain
  • Most common childhood physical disability
63
Q

Causes of Cerebral Palsy?

A
  • its not a diagnosis but a description–> Underlying diagnosis which lead clinical diagnoses of CP are: genetic, infections, bleeds/ clots, accidents/ injuries, hypoxia
  • Non- progressive damage to the developing brain – antenatal, perinatal or early postnatal period
  • Male > female; preterm; multiple birth; small for gestational age
  • Clinical presentation can change across the lifespan
64
Q

Define cognition & perception.

A

Cognition: Manipulation of information generated internally or externally
Perception: Interpretation of sensory information into psychologically meaningful information - Different regions within the brain: Prefrontal lobe & posterior parietal cortex

65
Q

What is the difference between lesions in the dominant VS non dominant hemisphere?

A
  • Left cerebral hemisphere is referred to as the dominant hemisphere (speech)
  • Right cerebral hemisphere is referred to as the non-dominant hemisphere
  • Left cerebral hemisphere damage can cause different cognitive/perceptual impairments to those caused from a right cerebral hemisphere lesion
66
Q

Explain Neglect. What happens and when does it occur?

A
  • Inability to attend to one side of the body & the environment on that side. Cannot interpret sensory info from the neglected side of body/ environment into psychologically meaningful info
  • More common in right (non-dominant) cerebral hemisphere lesions (more common to see left-sided neglect)
  • Typical behaviours observed relating to the individual, task and environment: bumping into this on left side, leaving food on left side of plate ect.
  • Other primary neurological impairments can contribute to the impact of neglect on the individual - L neglect, L loss of SS, L loss of visual field, L weakness (these can all compound neglect)
67
Q

What is dyspraxia/ apraxia?

A
  • Unique category of movement disorder in which the person is unable to carry out – on request and/or by imitation – a skilled, learned movement. E.g. ask them to go lying to sitting and they can’t do it (even though they psychically can do it automatically)
  • Difficulty in executing purposeful movements on demand despite adequate limb movements and sensation
  • Posterior Parietal cortex
68
Q

What is aphasia?

A
  • An impairment which describes the inability to either understand language or use language to express yourself.
  • Due to dysfunction of language areas in the frontal or parietal lobes
  • More common in left (speech dominant) cerebral hemisphere lesions
69
Q

What is Receptive aphasia?

A
  • Unable to understand written and spoken language and unable to speak or write with significant meaning
  • Language comprehension deficit
  • Due to lesions of Wernicke’s Area in the parietal lobe
  • Individuals usually unaware or less aware of the impairment
  • They think their communication makes sense
70
Q

What is Expressive Aphasia?

A
  • Able to understand written and spoken language but unable to speak or write with significant meaning
  • Single words comprehensible, sentences incomprehensible
  • Frontal Lobe dysfunction - Broca’s area
  • Individuals area aware of this impairment and have difficulty communicating – can appear frustrated
71
Q

Explain Pushers syndrome?

A
  • Impaired perception verticality (orientation body relative to gravity)
  • View upright approximately 20° to the affected side
  • Individual pushes with the unaffected side toward the affected side (Right-sided lesion will push from the right to the left (left is where the paresis is)

Neuroscience 2020 (2 decks)

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