Intro to Neuropath Flashcards
Glial Cell Type and Functions:
What protects the brain?
The blood brain barrier and the 3 meninges
Is the CNS ‘immune priveleged’?
- believed to have been shielded away from the
rest of the body’s immune response - however there may be a connection between
lymphatic system and brain
What is the main immune cell of the brain?
Where is it derived from?
Actions?
- microglial cell = APC
- from embryonic yolk sac progenitor cells
- major antigen presenting cells
- dendritic cells (checkpoint inhibitor)
Neuroinflammation:
- facilitates the delivery of effector molecules to
aid repair through signals - vascular dilatation = increased permeability =
alterations in adhesion - microglia activate and macrophages outside
the CNS are recruited - astrocytes repair
- demyelination
Neuroinflammation Flowchart:
Two types of neuroinflammation are:
- vasogenic = extracellular
- cytotoxic = intracellular
What is shown below?
Neuroinflammation
What is shown below?
Microglia (L-R)
1) resting
2) become activated, larger, higher turnover of
ATP = more circular, spherical cells
3) evidence of inflammation, larger, angrier
4) resting state in older patients; more worn
down cells, impairs function of microglia
Which types of oedema correspond to the CAT below?
- left is vasogenic, cellular ‘ boundaries are seen,
clear grey and white differntiation - right is cytotoxic and less clear differentiation
Chronic changes to neural damage (3):
- neural degeneration
- demyelination
- gliotic scars: possible epileptic foci
Retrograde Neural Degeneration:
when the main axon is damaged there is degeneration of the neurone as well as the classical distal degeneration of the axon
Trans-Synaptic Degeneration:
injured neurons spread injury to previously uninjured neurons connected by a synapse (diaschisis)
VITAMIN C:
What is a meningioma?
a tumour of the meninges
What is now used to define patient subgroups in oncology?
Molecular classification
precision cancer medication
Paraneoplastic Syndrome:
- remote effect of a cancer
- abnormal immune response to a cancer eg
lung/breast/ovarian - antibodies to T-cells begin to fight the normal
brain (AUTOIMMUNE) - symptoms develop over days to weeks
- involve peripheral (Lambert Eaton (small cell
lung cancer, causes weakness that improves
over time) or cns (NMDA encephalitis(presents
with psychosis but is actually ovarian tumour) - rare but presentation may be the first
symptom of an underlying malignancy
Meningoencephalitis:
- non-localised/diffuse problem
- meningitis = inflammation of the meninges
- presents as headache, nuchal rigidity (neck
stiffness), and photophobia
- leptomeninges (pia+arachnoid) = infection
- pachymeninges (arachnoid + dura) =
cancer (both are usually not always) - encephalitis = alteration in the
sensorium/cognitive state due to
inflammation (infection/autoimmune)
- drowsy, confused, less responsive
Decompression of the spinal compartment for example during a lumbar puncture could result in a brain herniation when
there is unequal pressures in the intracranial compartment eg cerebellar tumour
removal of fluid can cause the brain to fall and herniation
STOP = shift, trauma, obstruction, posterior fossa mass
Causes of Meningoencephalitis:
What are coup and contre-coup injuries?
direct and indirect
Traumatic Brain Injury: Blunt Force:
- concussion
- contusion
- secondary consequences of blunt force
trauma c
- concussion: clinical syndrome with immediate
and transient alteration in brain function can
result in headache, drowsiness, concentration
and amnesia for months - contusion: pathological term (seen on scan)
meaning bruising of the brain tissue, can result
in confusion, altered consciousness and focal
neurological deficits within days or weeks - due to moving the brain backwards = contre-
coup - eg boxer is punched and becomes blind, but
not because of punch to eye but due to
contusion at visual cortex at the back of the
skull - secondary effects:
- cerebral oedema and ischaemia
- vascular damage
Traumatic Brain Injury: Acceleration-Deceleration:
- examples of such injuries
- caused
- what scans are needed
- car accidents, shaken baby syndrome
- rotational movements of the brain in the skull
result in shearing forces causing axons to
stretch = diffuse axonal injury - can result in loss of consciousness or coma
- may need MRI with T2 flair images; may be a
delay in injury showing up on scan
Increased Cerebral Pressure:
- brain expands in very small space available
- results in herniation
- headaches, meningism, vision changes, CN6
palsy - high bp, redlexive bradycardia,, irregular
respiration = Cushings reflex (high bp, low
heart rate, erratic breathing)
Chronic Traumatic Encephalopathy:
- recurrent head injuries
- deposition of beta amyloid plaques. diffuse
plaques and tau mostly TAU - below pia mater
- was classified as a tauopathy
- present with dementia like features decades
after recurrent head injuries
Headaches: Categories:
- Primary: tension-type, migraine, trigeminal
autonomic cephalagias - Secondary: infection, neoplasm, stroke, meds,
toxins
Headaches: Red Flags:
- worsens with valsalva
- wakes you up whilst sleeping
- change in character:
- age of onset
- sudden onset
- focal neurological deficits
- constitutional symptoms: fever, weight loss,
meningism, rash
Mneumonic for headache history taking = SNNOOP10:
Primary Headaches: Tension-Type:
- 90% headaches
- featureless,, band-like pressure, stress
- pathophysiology is unknown
- episodic: frequent if at least 10 headaches on
1-14 days a month for >3 months - chronic: headaches on >14 days/ month for
>3months
Primary Headaches: Migraine:
- photophobia
- incapacity
- nausea/vomiting
- episodic: without aura, with aura ( visual:
zigzags, olfactory hallucinations) - chronic: at least 15 days/month for more than
3 months, which on at least 8 days a month
has the features of a migraine headache - status migrainosus: an attack lasting longer
than 72 hours
Primary Headache: TACs:
- trigeminal parasympathetic reflex with clinical
signs of cranial sympathetic dysfunction being
secondary - cluster headache: male predisposition,
excruciating pain causing agitation, autonomic
features - paroxysmal hemicrania
- short-lasting unilateral neuralgliform
headache attacks - hemicrania continua
Primary Headache: Summary:
Pathophysiology of Headache (Migraine):
- neurovascular theory
- sensory neurons of the
trigeminocervicocomplex is the source of pain
resulting in the release of inflammatory and
noiciceptive mediators which over time can
result in central sensitisation responses
Trigeminal Nerve: Sensory Pathway:
- 1st order
- 2nd order
- 3rd order = ventromedial nucleus of the
thalamus - 4th order = sensory cortex, insula, cingulate
cortex
trigeminal cervical complex is a physiological complex
probably one of the reasons there is neck pain and pain is not localised
Trigeminocervical Complex:
- physiological complex not anatomic
- how head and neck sensory information
combine - innervation of large cerebral vessels, pia
vessels, dura mater, large venous sinuses - anterior = mostly V1 (ophthalmic)
- posterior = mostly upper cervical roots
Trigeminal Autonomic Reflex pathway explains why
autonomic system activates running nose, eyes on the same side as the headache pain is felt
ipsilateral autonomic features from cranial parasymapthetic activation (lacrimation) and sympathetic hypofunction due to neurpraxic effect of the carotid wall swelling
afferent = trigeminal
efferent = superior salivatory nucleus via the 7th (facial) cranial nerve to synapse nicotinic post-ganglionic parasympathetic neurons)
We prevent medication overuse for headaches by
limiting monthly use of the medications eg
triptans < 10 days
non-opiod analgesics < 15 days
opiods < 10 days
chronic headaches should be managed with preventative strategies
Anoxic Brain Injury:
- hypoxia: drowning, strangulation, CO, asphyxia
- ischaemia: cardiac arrest, increased intracrania
pressure, hypovolaemia - may result in:
- seizures and myoclonus
- coma
- minimally conscious state
- unresponsive wakefulness syndrome
- brain death
What is shown below?
anoxic brain injury
Histopathology classifies the tumour but genotyping will dictate treatment in the future.
True or False?
True
