neuropathy Flashcards
how are neurons generated
how many neurons in brain?
What happens in neuroinflammation?
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Inflammation facilitates the delivery of effector molecules to aid repair though signals (cytokines eg interleukins)
1) Vascular dilatation, increased permeability, alterations in adhesion signal
2) Microglia become activated (histologically different)
- Macrophages can be recruited (from outside the CNS)
3) Oedema can be - vasogenic (extracellular)
- cytotoxic (intracellular)
4) Astrocytes repair (non-specific)
5) Demyelination [see Introduction to Demyelination]
what is visible in this image?
midline shift
what is wallerian degeneration?
Neural degeneration:
Retrograde / Wallerian degeneration when the main axon is damaged there is degeneration of the neurone as well as the classical distal degeneration of the axon.
what is trans-synaptic degeneration?
Trans-synaptic degeneration – injured neurons spread injury to previously uninjured neurons connected by a synapse [diaschisis]
name two types of neural degeneration?
Retrograde / Wallerian degeneration main axon damage = end axon damage
Trans-synaptic degeneration – sideways spread
Name three categories of neural damage
Neural degeneration
demyelination
gliotic scars - possible epileptic foci
what is a side-effect risk of gliotic scarring?
possible epileptic foci
does the pathology or the location determine the clinical symptoms?
Location - there can be multiple potential pathologies, but the location causes the clinical features
give 4 examples of neural pathology that can present as clinical symptoms
Neoplasm
Abscess / infiltrates (toxoplasmosis, neurocystercicosis)
Stroke
Trauma (but can result in a contrecoup injury)
What does the mnemonic “VITAMIN C” stand for when ddx-ing pts?
V
I
T
A
M
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C
V-ascular
I-nflammation/infectious
T-oxins/drugs
A-utoimmune
M-etabolic
I-diopathic
N-eoplastic
C-ongenital/genetic
“Cell type is determined by histopathology though location can be helpful in differential…” of what?
neoplasms
imaging over time can help, or observing other
What type of neoplasm is most common in Brain?
Metastasis - they ‘land’ at the grey-white jct as the vascular border zone, presumable having travelled form the body through blood
What sort of neoplasm is this showing?
Meningioma - tumour of the meninges. Invades/compresses
can you name these? (hard, not nessecary?nessecary??)
Is histopathology the main approach to classify tumours?
Histopathology was the main approach to classifying gliomas along their predominate cell type and grading their malignancy
Now molecular classifications define patient subgroups that have better prognosis within a specific histology and grade
Is histopathology the main approach to classify tumours?
Histopathology was the main approach to classifying gliomas along their predominate cell type and grading their malignancy
Now molecular classifications define patient subgroups that have better prognosis within a specific histology and grade
What is molecular targeting
Quasi-uniqueness of the patient and their tumour genetics (molecular targeting)
What is molecular targeting
Quasi-uniqueness of the patient and their tumour genetics (molecular targeting)
How does “mathematical neuro-oncology” work?
to predict and quantify response to therapies
How does immunotherapy help in neuro-oncology?
What are the risks/problems with it?
Immunotherapy harnesses the power of the immune system to fight brain tumours
Limited space for an inflammatory response, difficulty with repeated sampling, use of steroids for oedema made this more challenging to use in the CNS
Previously most useful for metastatic tumours from solid cancers eg melanoma and non-small cell lung cancer but now being used for GBM
what is a paraneoplastic syndrome?
neurological symptoms of a non-neurological problem
e.g.Remote effect of a cancer
Abnormal immune responses to cancers eg lung, breast, ovarian
Antibodies or T-cells begin to fight the normal brain (autoimmune)
Symptoms develop over days to weeks
Symptoms involve the peripheral (Lambert Eaton) or central nervous system (NMDA encephalitis)
Rare but their presentation may be the first symptom of an underlying malignancy
what is meningoencephalitis and two sub-named conditions?
Non-localized/diffuse problem
Meningitis – headache, nuchal rigidity, photophobia
inflammation of the leptomeninges [pia + arachnoid] is usually infection
Inflammation of the pachymeninges [arachnoid + dura] is usually cancer or tuberculosis
Encephalitis – alteration in the sensorium/cognitive state due to inflammation (infectious / autoimmune)
when are lumbar punctures indicated?
lumbar puncture/spinal tap is a diagnostic tool - can be vital to confirm or deny where an infection is or what sort of infection
-Opening Pressure
-Cell type (red, white, other)
-Glucose levels
-Protein levels
-Colour
-Culture, PCR, antibodies
Where do you place need in lumbar puncture?
Intercristal plane (iliac crest place, above spine of L4)
this should ensure the needle pierces into cauda equine area and not into spinal cord (neurological damage) to tap some CSF for sampling.
Lower down the vertebrae are too close together and it can be difficult to insert the needle
Local anaesthetic needed!
What should you be concerned about when performing lumbar puncture?
Don’t STOP (shift, trauma, obstruction, posterior fossa mass)
there may be considerable danger when lumbar puncture is performed in the presence of increased intracranial pressure,
-unequal pressures in the intracranial compartment could result in brain herniation following decompression of the spinal compartment
Meningoencephalitis lumbar puncture:
If the CSF pressure is high, appears turbid, protein high, serum glucose is low, and WC: neutrophils are present, what is suspected?
Bacterial infection
what do you do if pt has viral encephalitides?
Underlying pathogen dictates treatment
Most viral encephalitides is supportive treatment
(many viruses have no specific treatment)
Meningoencephalitis
Lumbar puncture results:
pressure is high/normal, appears clear, protein normal-high, serum glucose is normal, and WC: lymphocytes are present, what is suspected?
Viral or aseptic
Most likely bacterial pathogen in meningeoencephalitis: neonates?
Neonates: E. Coli, group B Strep
Most likely bacterial pathogen in meningeoencephalitis: infants/young children?
Infants and children: Haemophilus influenza & Neisseria meningitidis
Most likely bacterial pathogen in meningeoencephalitis: adolescents/young adults?
Adolescents / young adults: Neirsseria meningitidis
Most likely bacterial pathogen in meningeoencephalitis: elderly?
Elderly: Streptococcus pneumoniae & Listeria monocytogenes
Most likely bacterial pathogen in meningeoencephalitis: alcoholics/diabetics/immunocompromised?
Alcoholics, diabetics, immunocompromised: Listeria
viral pathogens in meningeoencephalitis?
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Viral
Unknown
Herpes (HSV 1, HSV 2, CMV, EBV, VZV)
Coxsackie
Polio
Echo
HIV
Rabies
Covid-19
What is brain sag?
CSF Too low pressure
Leak (trauma or spinal tap) causing brain sag
what can cause CSF pressure to be too high?
Too high pressure
Blockage of flow (stenosis, colloid cyst, subarachnoid hemorrhage, meningitis, venous sinus thrombosis)
Over production (choroid plexus papilloma)
Reduced reabsorption (neoplasms, congenital malformations)
what can cause CSF pressure to be too high?
Too high pressure
Blockage of flow (stenosis, colloid cyst, subarachnoid hemorrhage, meningitis, venous sinus thrombosis)
Over production (choroid plexus papilloma)
Reduced reabsorption (neoplasms, congenital malformations)
What does “leptomeninges” mean?
both Pia and arachnoid mater
what does pachymeninges mean?
arachnoid and dura mater
What are the blue foramina called?
foramina of Lushka (2) and magendie(1)
what do the foramina of Lushka (2) and magendie (1) do?
The median aperture (foramen of Magendie) opens on midline into a subarachnoid space inferior to the cerebellum called the cisterna magna and into the quadrigeminal cistern in the region of the tectum of the midbrain. Two lateral apertures (foramen of Luschka) also open into the cisterna magna.
how many foramen drain CSF from ventricles of Brian?
Lushka (2) and magendie (1) do?
Which side of this image set is normal L or R?
R is Hydrocephalus on imaging, L is normal
What are coup/contre-coup injuries?
Blunt force traumatic brain injuries, Coup (direct) and contre-coup (indirect) injuries
What is concussion?
Concussion - a clinical syndrome with immediate and transient alteration in brain function can result in headache, drowsiness, concentration and amnesia for months (post-concussive syndrome)
What is contusion?
Contusion – a pathological term meaning bruising of the brain tissue and can result in confusion, altered consciousness, and focal neurological deficits immediate or some time later (days – weeks)
Secondary effects of blunt trauma?
cerebral oedema (and ischaemia)
blood vessel damage
Secondary effects of blunt trauma?
cerebral oedema (and ischaemia)
blood vessel damage
What is an accel-decel traumatic brain injury?
Rotational movements of the brain in the skull result in shearing forces causing axons to stretch (diffuse axonal injury) and can lead to loss of consciousness or coma.-can cause demyelination damage?
E.g. motor vehicle accidents or shaken baby syndrome
Will accel-decel injuries be seen by imaging?
CT scans of the head often don’t show evidence of diffuse axonal injury. Magnetic resonance imaging (MRI )of the brain with T2-flair images is needed and may demonstrate punctate hyperintensities at the gray-white junctions or within the brainstem
How might ICP present?
Increased cerebral pressure (ICP)
Headaches, meningism
Vision changes, papilloedema, CN6 palsy (due to meningeal effects not CN6 specific)
Loss of consciousness
High blood pressure, reflexive bradycardia
(baroreceptors), irregular respirations = Cushing’s
reflex
What is “Cushing’s reflex”?
really bad sign of ICP
High blood pressure, reflexive bradycardia
(baroreceptors), irregular respirations
what is Chronic Traumatic Encephalopathy?
Known about since 1920s – punch-drunk syndrome or dementia pugilistica and Characterized in 2000s in athletes - research ongoing (repeated head traumas, pathology seen by autopsy)
Tauopathy with preferential involvement of the superficial cortical layers prominent perivascular, periventricular, and subpial distribution, and marked accumulation of tau-immunoreactive astrocytes.
Deposition of β-amyloid, most commonly as diffuse plaques, occurs in fewer than half the cases.
What conditions have tauopathy
Chronic traumatic encephalopathy (CTE)
Progressive supranuclear palsy (PSP)
Corticobasal degeneration (CBD)
what conditions are linked with amyloidopathy?
Alzheimer’s disease (AD)
Cerebral amyloid angiopathy (CAA)
Posterior cortical atrophy
Agrammatic primary progressive aphasia
what conditions are linked with synucleinopathy?
Parkinson’s disease (PD)
Dementia with Lewy bodies (DLB)
Multiple System atrophy (MSA)
prion disease conditions?
New variant Creutzfeldt Jakob disease (v-CJD)
Kuru
TAR DNA-binding protein 43 (TDP-43)
Motor neuron disease (MND) /
Amyotrophic lateral sclerosis (ALS)
HEADACHE
