Neuro Week 7

Neurological disorders, neuroimaging, and pain

When neurologic signs or symptoms are present, consider;

1. what happened

2. when did it begin

3. how has it changed

4. what functions are affected

5. what pattern do the findings suggest

6. where might the nervous system be involved

lesion

an area of pathologic tissue resulting from disease or injury

the effects of a lesion depend on

1. location

2. size

3. structures/pathways involved

location helps us connect neurologic …….

damage to function

A lesion in the primary motor cortex would impair…

voluntary motor control

a lesion in the occipital cortex would impair…

vision (post chiasm lesion)

a lesion in the cerebellum would impair…

coordination/balance/real time error correction

a lesion in the brainstem would impair…

autonomic function/cranial nerves/issues with ascending and descending tracts

focal lesion

limited to a single location

multifocal lesion

several separate, nonsymmetric locations

diffuse lesion

widespread involved, often affecting structures bilaterally

(TBIs)

multiple areas of demyelination involving different CNS locations would be from a what kind of lesion

multifocal lesion

A single cerebral infarct affecting one vascular territory would be a what kind of lesion

focal lesion

widespread brain dysfunction following global hypoxia would be what kind of lesion

diffuse lesion

incidence =

new

prevalence =

existing

Incidence

new cases occurring within a defined population over a specified period of time

Prevalence

existing cases within a defined population a particular time

50 people develop MS this year =

incidence

200 people are currently living with MS =

prevalence

speed of onset does or does not equal pattern of progression

does NOT equal

speed of onset

• how quickly did the symptoms begin

  • and reach their peak

• types

  • acute

  • subacute

  • chronic

pattern of progression

what happened to the symptoms after they began

Acute speed of onset

minutes to hours to maximal signs and symptoms

Subacute speed of onset

progresses to maximal over a few days

Chronic speed of onset

gradual worsening continuing for weeks or years

Acute pattern of progression

often stable or improving

Subacute pattern of progression

fluctuating or gradual improvement

Chronic pattern of progression

may progressively worsen

important information for neurologic examination;

1. speed of onset

2. pattern of progress

3. mental status

4. distribution and pattern of symptoms

important information to consider regarding mental status;

1. is the person awake

2. is the person aware

3. can the person respond appropriately to question

history + examination + testing =

clinical reasoning

History to hypothesis pathway

1. history

2. pattern of signs and symptoms

3. possible region of nervous system involvement

4. testing/additional diagnostic information

   1. neuroimaging

5. diagnosis

What can neuroimaging tell us?

1. visualize nervous-system anatomy

2. identify structural abnormalities

3. examine blood vessels

4. examine aspects of neural function

5. relate lesion location to clinical presentation

Axial (transverse/horizontal) THINK

looking from the feet toward the head

Coronal (divides anterior/posterior portions) THINK

looking face to face

Sagittal (divides right/left portions) THINK

side view

CT (computed tomography)

• uses x-rays

• rapid

• useful for acute hemorrhage, fractures, and other abnormalities

• ionizing radiation exposure

MRI (magnetic resonance imaging)

• uses magnetic fields and radiofrequency signals

• may be contraindicated with certain metal/implanted devices

• greater soft tissue detail

• useful for many CNS lesions/disorders

• longer scan time

• no ionizing radiation

CT THINK

density

Hypodense (CT) color

Darker (CSF/air)

Hyperdense (CT) color

Lighter/brighter (bone)

CT darker to bright

air → CSF → white matter → gray matter → acute blood → bone

MRI THINK

Signal intensity

Hyperintense (MRI) color

brighter (higher signal) (CSF)

Hypointense (MRI) color

darker (lower signal)

Types of MRIs

T1 and T2

T1

CSF - Dark

White matter - Light grey

Gray matter - Dark grey

Edema - Dark

T2

CSF - Bright

White matter - Darker gray

Gray matter - Lighter gray

Edema - Bright

Specialized MRI; FLAIR (fluid attenuated inversion recovery)

• a type T2 imaging

• suppresses the CSF signal

• abnormal tissue with increased water content (e.g., edema) can remain bright)

• makes abnormalities adjacent to CSF easier to see

• EX; MS

Specialized MRI; DWI (diffusion-weighted imaging)

• sensitive to the movement (diffusion)

• particularly useful for identifying; acute ischemic

• ischemia → cells swell → water movement restricted → visible on DWI

• clinical connection

  • DWI can show changes within minutes after cerebral ischemia - recall stroke as an acute-onset, vascular disorder

Specialized MRI; DTI (diffusion tensor imaging)

• uses patterns of water diffusion (water tends to move preferentially along axon bundles) to examine

  • white matter organizes

  • direction/orientation of fibers pathways

  • integrity of neural tracts

• Think; where do the white-matter pathways go

• Rehab connection

  • has documented corticospinal tract changes following constraint-inducing movement therapy

What does the nervous system look like

structural imaging

(CT & MRI)

what is the nervous system doing

functional imaging

(PET & fMRI)

PET (positron emission tomography)

• uses radiotracers (injected radioactive isotopes)

• examines physiologic / metabolic activity (blood flow, glucose metabolism, oxygen use)

fMRI (functional MRI)

• uses changes associated with blood oxygenation

• maps activity associated with brain function

• no radioactive injection

structures matter - but so do…

1. neural processing

2. sensitization

3. plasticity

4. descending modulation

5. context

Acute pain

• normally serves a protective function (a warning sign)

• often associated with injury/tissue damage

Chronic pain

• persists (or recurs) for greater than/equal to 3 months

• may involve persistent changes in nervous system processing

• can be split

  • primary pain

  • secondary pain

Chronic primary pain

• pain is the principal condition

  • not explained by a clearly identifiable tissue injury

• examples

  • fibromyalgia

  • chronic nonspecific low back pain

  • CRPS

    • complex regional pain symptom

  • migraine

Chronic secondary pain

• pain occurs in association with (as a symptom of) another underlying disease or injury

• neuropathic

  • small fiber neuropathy

  • phantom limb pain

• nociceptive

  • arthritis

  • cancer pain

  • myofascial pain

  • post-surgical/post traumatic

central sensitization

increased responsiveness (excessive excitability) of nociceptive neurons in the CNS

normal nociceptive input → changes in CNS → ?

amplified response

Mechanisms of central sensitization

• increased excitability

  • neurons respond more strongly to the same input

• structural reorganization

  • rewiring of connections, including in the cortex

• reduced descending inhibition

  • less “turn down” signaling from the brain

  • less antinociception

• increased descending facilitation

  • more “turn up” signaling from the brain

  • more pronociception

hyperalgesia

increased pain response to a normally painful stimulus

allodynia

pain due to a stimulus that is normally nonpainful

temporal summation

increased pain response with repeated (or continued) stumulation

secondary hyperalgesia

increased pain sensitivity beyond the original area of injury

Fibromyalgia common characteristics

1. widespread pain (and stiffness)

2. fatigue

3. sleep disturbance (nonrestorative sleep)

4. heightened sensitivity

5. may include cognitive (concentration, memory) and other symptoms

Fibromyalgia neuroscience connection

• evidence supports altered central pain processing, including;

  • central sensitization

  • reduced pain inhibition (less activity in pain-inhibiting brain areas)

  • altered responses to sensory input (pressure reported as painful)

Migraine

• a brain based neurologic condition characterized by episodic headache and associated symptoms

• phases overlap, and not every person experiences every phase

• phases

  • prodrome

  • aura

  • headache

  • postdrome

• associated symptoms

  • sensory sensitivity (light, sound, smell), nausea, and neurological symptoms

• neuroscience connection

  • involves alter nervous-system processing; central sensitization may contribute to heightened sensory and pain sensitivity

Phases of a migraine

• prodrome

  • several hours - days

  • hypothalamus activation

  • yawning, food cravings, irritability

• aura

  • 5 min-1 hours

  • cortical spreading depression

  • visual disturbances, numbness/tingling

• headache

  • 4 hours - 3 days

  • trigeminal pain pathway activation

  • head/neck pain, nausea, light/sound sensitivity

• postdrome

  • 1-2 days

  • decreased brain blood flow

  • mood change, difficulty concentrating

CRPS persistent regional pain that may include;

1. pain disproportionate to the inciting event

2. hyperalgesia/allodynia

3. edema

4. skin color or temperature changes

5. autonomic changes (sweating)

6. motor dysfunction

Regional

• usually one limb, often worst distally; commonly follows trauma (e.g., fracture, surgery, sprain)

CRPS neuroscience connection

• inflammation in the early (“warm”) phase

• central sensitization

• possible sympathetic (autonomic) and immune dysfunction

• cortical reorganization

• mirror therapy

possible cortical changes in CRPS

• cortical reorganization

  • representation of the affected limb in sensory and motor cortex may change

• altered brain activity

  • in areas associated with pain, sensation, and emotion

Chronic nonspecific low back pain

persistent low-back pain without one clearly identifiable, specific pathoanatomic cause

chronic nonspecific low back pain may be influenced by;

• nociceptive input

• altered pain processing

• movement/activity

• psychological factors

• environmental/social factors

Chronic nonspecific low back pain key concept

pain severity does not necessarily correspond direct to identifiable tissue damage

Neuropathic pain

pain caused by a lesion or disease of the somatosensory nervous system (a type of chronic secondary pain)

neuropathic pain may be described as

• burning

• shooting

• electric

• tingling

• painful sensitivity

paresthesia

abnormal but painless sensation

neuropathic pain may result from damage to the _______ or _______ central somatosensory nervous system

peripheral, central

Peripheral neuropathic pain

lesion/disease affecting the peripheral somatosensory nervous system

Examples

• peripheral neuropathies (diabetic peripheral neuropathy)

• nerve injuries / compression (sciatica, carpal tunnel syndrome)

Central neuropathic pain

lesion/disease affecting the central somatosensory nervous system

Examples

• can occur following CNS injury or disease

  • spinal cord injury, post stroke pain, multiple sclerosis

A client reports widespread pain, fatigue, poor sleep, and heightened sensitivity to touch

fibromyalgia

Following a wrist injury, a client develops sever hand pain, swelling, temperature/color changes, and pain with light touch

CRPS

A client with a median nerve injury describes burning and electric sensation along the affected nerve distribution

neuropathic pain (peripheral)

biological

1. nervous-system changes

2. injury/disease

3. genetics (and sex)

4. physical conditioning

5. sleep patterns

Psychologicial

1. thoughts / beliefs (catastrophizing)

2. mood (anxiety, depression)

3. attention to pain

4. coping skills

Social

1. environment and healthcare access

2. relationships and support

3. work / roles

4. social context and expectations

managing chronic pain

Often interdisciplinary

• pharmacologic

  • medication management

  • several drug classes are used; none is effective for everyone

• nonpharmacologic/rehabilitation

  • exercise and physical activity

  • education (pain neuroscience education)

  • behavioral / psychological approaches (CBT, relaxation)

  • rehabilitation interventions

pain can disrupt

1. ADLs

2. IADLs

3. Sleep

4. Work/school

5. Physical activity

6. social participation

7. roles and routines

OT may address

1. occupational participation

2. activity modification

3. graded return to meaningful activity

4. routines and habits

5. self-management

6. environmental / contextual barriers

Pieces together

1. signs and symptoms

2. history + onset + progression

3. clinical reasoning

4. localization + neuroimaging

5. nervous system processing

6. function and occupation

nervous system processing can influence the relationship between _______ and ______

pathology, function