Prosencephalon becomes
Telencephalon > Cerebrum Diencephalon > Thalamus and Hypothalamus
Mesencephalon becomes
Midbrain
Rhombencephalon
Metencephalon > Pons and Cerebellum
Myelencephalon > Medulla
Ascending Pathways are
Somatosensory
2 Ascending pathways
- Spinothalamic Tract
- Dorsal Column Medial Leminiscus (DCML)
Spinothalamic Tract is responsible for
Pain and Temperature
Spinothalamic fibres decussate at
Spinal cord
A lesion in the spinothalamic tract would cause
Contralateral loss of pain and temperature
Spinothalamic tract is
Anterior
DCML Pathway is responsible for
Fine touch, pressure and vibration
DCML fibres decussate in
the medulla
A lesion in the DCML pathway would cause
ipsilateral loss of fine touch, pressure and vibration sensations
DCML pathway is
Posterior
DCML is split into
- Fasciculus cuneatus: Upper limbs and trunk
- Fasciculus gracilis: Lower limbs and trunk
“You stand with grace”
Fasiculus Cuneatus ends at
T6
Descending pathways are
Somatomotor
2 main descending pathways
- Pyrimidal (Corticospinal, Corticobulbar)
- Extrapyrimidal (Reticulospinal, Rubrospinal)
Pyramidal Tracts are
Anterior
Extrapyramidal tracts are
Anterior
Corticospinal tract is split into
- Lateral corticopsinal tract
- Anterior corticospinal tract
Lateral Corticospinal tract is responsible for
Voluntary motor control of the limbs and digits
Lateral corticospinal fibres decussate in the
Medulla (pyramidal decussation)
A lesion in the lateral corticospinal tract would cause
Weakness in ipsilateral limbs and digits
Anterior corticospinal tract is responsible for
Voluntary motor control of the trunk (maintains posture)
Corticobulbar tract is responsible for
Motor control of the muscles of the face, head and neck
Corticobulbar tract is associated with
Cranial Nerves
Rubrospinal tract
controls flexion in the upper limbs
“RuBROspinal as they are bicep curling”
Origin of rubrospinal tract is in the
red nucleus (in the midbrain)
Reticulospinal tract
excites extensor muscles
Decerebrate posture
- Extension of all upper and lower limbs
- Pronation of the wrist
- Damage to brain, including midbrain
“You De-celebrate because they are dead, or look like it”
Decorticate
- Flexion of upper limbs
- Extension of the lower limbs
- Damage to brain, excluding midbrain (rubrospinal is intact)
“Your arms are flexed to your deCOREticate”
- Ipsilateral loss of touch, pressure, vibration
- Ipsilateral loss of motor strength
- Contralateral loss of pain and temperature
Brown Sequards Syndrome
“Hemi-section of the cord”
Bilateral loss of touch, pressure and vibration
Posterior Cord Syndrome
- Bilateral loss of pain and temperature in a cape-like pattern
- Bilateral weakness in proximal upper limbs
Central Cord Syndrome
- Bilateral loss of motor strength
- Bilateral loss of pain and temperature sensation
Anterior Cord Syndrome
- Bilateral loss of touch, pressure and vibration
- Bilateral loss of pain and temperature
- Bilateral loss of motor strength
Complete Cord Sydnrome
Muscle weakness is a sign of
Upper and lower motor neuron lesion
Muscle atrophy is
LMN lesion
“Loss of muscle = Lower”
Hyperreflexia is
UMN lesion
Hyporeflexia is
LMN lesion
Increased tone
UMN lesion
Decreased tone
LMN lesion
Fasciculations
LMN lesion
Babinski sign is positive
UMN lesion
Types of Motor Neurone Disease (MND)
- Amyotrophic Lateral Sclerosis (ALS)
- Primary Lateral Sclerosis (PLS)
- Progressive Muscular Atrophy (PMS)
- Spinal Muscular Atrophy (SMA)
ALS
UMN and LMN lesions
At the beginning ALS involves
upper limbs (starts distally)
Frontotemporal Dementia is seen in
ALS
The gene that links FTD and ALS is
C9ORF gene
Treatment to improve survival in ALS
Riluzole
Treatment to improve spasticity in ALS
Baclofen
Treatment to reduce the viscosity of sputum in ALS
Carbocisteine
Primary Lateral Sclerosis presents with
UMN symptoms
Progressive Muscular Atrophy presents with
LMN symptoms
Spinal Muscular Atrophy presents with
LMN symptoms
“Floppy Baby Syndrome” - hypotonia
Gene for SMA
SMN 1 gene
Cyst in spinal cord
Syringomyelia
- Sensory loss (pain and temperature) in the upper limps and “cape” area
- Paralysis
- Muscle weakness
- Neck pain
- Bladder problems
Syringomyelia
- Sciatica
- Lower back pain
- Lower Limb/buttocks loss of sensation/ tingling
Lumbar stenosis
Compression of the spinal cord
Spinal Stenosis
Pain relieved on sitting forward or walking uphill
Lumbar stenosis
Spinal cord stops at
L1/2
Lumbar punctures are taken at
L3/4
Intervertebral disc prolapse causing Cauda Equina Syndrome usually happens at
L4/5
- Lower limb weakness/ pain/ loss in sensation
- Saddle area anaesthesia
- Bladder/bowel incontinence
Cauda Equina Syndrome
- Unliateral mydriasis (dilated pupil)
- Down and out eye
- Ptosis (drooping eye lid)
Third Nerve Palsy
- Facial drooping
- Loss of forehead wrinkles
- Inability to close eye
- Inability to produce tear film (dry eyes)
- Hyperacusis (stapedius)
Bell’s Palsy (Facial Nerve palsy)
Treatment for Bell’s Palsy
Steroids
- Miosis (constricted pupil)
- Partial ptosis
- Enophthalmos (sinking of the eyeball in socket)
- Ipsilateral anhidrosis
Horner’s Syndrome
Horner’s Syndrome is due to
Sympathetic nerve problem/damage
- Damage to C5/C6
Erb’s Palsy
- Internally rotated arm
- Pronated forearm
- Flexed wrist
“Waiters tip posture”
Erb’s Palsy
Damage to C8 and T1
Klumpke’s Palsy
“Claw hand”
Klumpke’s Palsy
- Muscle fatigue at the end of the day
- Diplopia, ptosis, heavy head
Myasthenia Gravis
Myasthenia Gravis pathophysiology
- Autoimmune neuromuscular junction disorder (B-cell mediated)
- Auto-antibodies attack post-synaptic Acetylcholine receptors
Myasthenia Gravis Antobodies
Anti Acetylcholine receptor antibodies (AChR)
(Produced in thymus)
1st line Treatment for Myasthenia Gravis
Pyridostigmine (Acetylcholinesterase inhibitor)
2nd line for myasthenia gravis
Thymectomy
Side effect of Pyridostigmine
Can cause a cholinergic crisis
Tx: Plasmapheresis and Ig
- Distal proximal weakness in arms and legs
- Pins and needles in hands and feet
- Recent GI campylobacter infection
Guillain-Barré Syndrome
Guillain-Barré Syndrome
Autoimmune destruction of peripheral nerves and their myelin insulation
Guillain-Barré Syndrome Antibodies
Anti-ganglioside antibodies
Treatment for Guillain-Barré Syndrome
Immunoglobins
- “Wine bottle legs/stork like legs”- like a saber tooth
- “Claw hand”
- “Hammer toe”
- Foot drop
Charcot-Marie-Tooth Disease
Pathophysiology of Charcot-Marie-Tooth disease
Motor and sensory neuropathies of the peripheral nervous system with associated muscle loss
Lambert-Eaton Myasthenis Syndrome
Muscle weakness to the limbs due to autoimmune antibodies attacking presynaptic Ca2+ channels, interfering with cell signals from nerve cells
Voltage gate calcium channel antibodies (VGCC)
Lambert-Eaton Myasthenic Syndrome
Lambert-Eaton Myasthenic Syndrome is associated with
Small cell carcinoma (lung cancer)
Treatment for Lambert Eaton Syndrome
- 3,4-Diaminopyridine +Steroids
- Pyridostigmine
- Optic neuritis
- Incontinence
- Ataxia
- Weakness
- Spasticity
- Pyramidal Dysfunction (Weakness in UL extensors, weakness in LL flexors)
Symptoms separated in space and time
Increasing frequency of symptoms
Relapsing and remitting disease
Multiple Sclerosis (MS)
Pathophysiology of MS
- Inflammatory process of demyelination of CNS
- Deposition of plaques around lateral ventricles “dawson’s fingers”
- Acute: Pink
- Chronic: Pearl grey
*
Lhermitte’s Sign
Movement of neck sends electric shock pain down spine
Present in MS
Investigations for MS
- MRI: lesions will be seen
- LP: Oligoclonal Bands seen in CSF
Raised Lymphocytes in CSF
Acute treatment of MS
High dose steroids (methylprednisolone)
1st line Treatment for MS
- Beta-interferon (Avonex, Extavia)
- or sometimes Copaxone
2nd line for MS
- Natalizomab (Monoclonal antibody)
- or sometimes Fingolimod
MS treatment for fatigue
Amantidine
MS treatment for increased sleepiness
Modafinil
MS treatment for spasticity
Baclofen, botox
Type types of Seizure
- General (all of the brain)
- Focal (partial bits of the brain)
Types of generalised seizures
- Tonic-clonic
- Myoclonic
- Myotonic
- Atonic
- Absence
Tonic-Clonic Seizure
- Tonic: Muscles tense up
- Clonic: Convulsions and shaky movements
Often bite tongue
Myotonic seizure
Muscles tense up
Myoclonic Seizure
Clonic jerks: Shaky movements
Common in kids, often happen in the morning
Atonic seizure
All muscles lose tone
They fall to the floor like in Toy Story
Absence seizure
Motionless stare for 15-30s
Types of Focal/Partial Seizures
- Simple: Remains consciousness
- Complex: Loss of consciousness + Aura
Classifications of Focal/Partial Seizures
- Frontal
- Temporal
- Parietal
- Occipital
Frontal Seizure
Motor signs: Twitching movements, stiffness
Temporal Seizure
- Deja Vu feeling
- Weird smell / taste
- Lip smacking
- Feeling of impending doom
Parietal Seizure
Loss of sensation in distal limbs
Burning / tingling sensation
Occipital Seizure
Visual problems
Todd’s Paralysis
A period of temporary paralysis following a seizure
Can last up to 24hrs
Investigation for someone having a seizure
ECG
1st line treatment of Generalised Seizures
Sodium Valproate
2nd line treatment for Generalised Seizures
Lamotrigine
Myoclonic: Levetiracetam
Absence: Ethosuximide
1st line treatment for Focal/Partial Seizures
Carbamazepine
2nd line treatment for Focal/Partial Seizures
Lamotrigine
or sometimes Levetiracetam
Contraindications for sodium valproate
- Teratogenic (don’t use in pregnancy), but can use in breastfeeding
- Weight gain
- Hair loss
- Fatigue
Contraindications of carbamazepine
Makes general seizures worse
Side effects of Lamotrigine
Dizziness and a rash
Contraceptive contraindications of Epileptic medications
- POP won’t work
- Increase dosage of COC
- Take 5mg Folic Acid for pregnancy
Status Epilepticus
- Single epileptic seizure lasting more than five minutes
- Two or more seizures within a five-minute period without the person returning to normal between them
Acute treatment of Status Epilepticus
1st: Rectal Diazepam, IV Lorazepam
2nd: Phenytoin
Single seizure patient can’t drive for
6 months
Single Seizure patient who drives heavy goods vehicles can’t drive for
5 years
Epilepsy patient without seizures has to wait
1 year of being seizure free to drive again
Epilepsy patient who drives a heavy goods vehicle has to wait
10 years seizure free while off of their medication
4 main types of Dementia
- Alzheimer’s
- Frontotemporal “Picks disease”
- Vascular
- Lewy Body’s
Criteria for dementia
2 or more of:
- Forgetfulness
- Memory loss
- Confusion
- Poor reason
- Personality changes
- Decreased concentration
- Visual perceptions
Tools for diagnosing Dementia
- 4AT
- MMSE
- MOCA
Frontal lobe is responsible for
Sequencing, fluency and behaviour
Parietal lobe is responsible for
- Language- Left side
- Spacial awareness- Right side
Temporal lobe is responsible for
Memory and speech
Alzheimer’s criteria
a decline in function in 2+ areas
Pathophysiology of Alzheimer’s Dementia
- Deposition of amyloid plaques (alphabeta) that are neurotoxic and cause an inflammatory response when broken down
- Deposition of Tau protein which is also neurotoxic
Alzheimer’s effects
Frontal, temporal and parietal lobes first
Starts in nucleus basalis of meynert
Amyloid plaques and Tau Protein cause
- Decrease in ACh which leads to less serotonin
- Decrease in GABA which leads to less NorA
Pathological changes to the brain in Alzheimer’s
- Huge sulci
- Narrowed gyri
- Cortical atrophy
- Thin brain
- Dilated ventricles
Genes associated with Alzheimer’s
- PSE1/2 is found in early onset dementia
- APP is found in Trisomy 21
Treatment for Alzheimer’s Dementia
- ACh inhibitor (Donepezil, Rivastigmine, Galantamine)
- Memantine (NMDA receptor antagonist)
Pathophysiology of Frontotemporal Dementia
- Deposition of Tau proteins- silver staining “Pick Bodies”
- Frontal lobe atrophy
- Gyral atrophy with knife-blade appearance
Do not offer
ACh receptor antagonists or memantine in Frontotemporal dementia
Presentation of Frontal temporal dementia
- Early insidious onset
- Personality changes
- Preserved memory
Lewy Body Dementia is caused by
- Deposition of Lewy bodies (alpha-synuclein)
Ubiquitin detects
Lewy bodies when stained
Lewy Body Dementia is associated with
Parkinson’s Disease
To have DWLB (Dementia with Lewy Bodies) and not Parkinson’s you must have
Onset of dementia symptoms within 1 year of onset of Parkinson’s symptoms
Presentation of DWLB
- Parkinson’s symptoms
- Visual Hallucinations
- REM Sleep disorder
Investigations for DWLB
Positive DAT (Dopamine active transporter) scan
Treatment for DWLB
ACh inhibitor (Donepezil, Rivastigmine, Galantamine)
Vascular Dementia pathology
- Multiple lacunar infarcts in small vessels in brain
Vascular Disease is found in
CHD/stroke patients
Vascular Dementia has a
Step wize progression
Dementia Pugilistica is found in
Boxers
Due to repeated trauma
Pathophysiology of Parkinson’s Disease
- Lewy bodies also aggregate in the brain and destroy the substantia nigra (produces dopamine)
- Decrease in dopamine leads to the inhibition of the thalamus (motor cortex) which in turn inhibits motor movement
Core features of Parkinson’s Disease
- Bradykinesia (causes shuffling gait)
- Resting Tremor
- Rigidity (cogwheeling limbs)
Other associated features with Parkinsonism
- Quiet speech
- Decreased facial expressions
- Decreased sense of smell
- Bladder dysfunction
Genes associated with Parkinson’s
- LRRK2 gene
- PRKN gene
Investigations for Parkinson’s
- Positive DAT scan
- Treatment with Levodopa will work- diagnostic
1st line treatment for Parkinson’s
Levodopa
(Carbidopa is prescribed alongside to prevent Levodopa from being broken down before it reaches the brain)
2nd line treatment for Parkinson’s
- Monoamine Oxidase Inhibitors (MAOIs): Selegiline, rasagiline
- Dopamine agonist (D2 receptor agonists): Pramipexole, Ropinirole, Bromocriptine
- COMT inhibitor: Entacapone
1st line treatment for Parkinson’s tremor
Anticholinergics
Parkinsons Plus
Parkinson’s plus additional neurodegenerative features
Parkinson’s Plus features
- Multi-system atrophy: Decreased BP, Ataxia
- Progressive supranuclear palsy: Vertical gaze, Hummingbird sign
- Cortical Basil Degeneration: Alien hand syndrome
Huntington’s disease
Progressive degeneration of striatium, basal ganglia, and cerebral cortex due
Huntington’s Genetics
Autosomal dominant
>38 glutamine (CAG repeats)
Chromosome 4
- The more repeats, the earlier the onset
- CAG repeats get longer in men, shorter in women
Huntington’s Presentation
- Middle aged
- Chorea
- Progressive dementia
Treatment for Huntington’s
Tetrabenazine (monoamine depletor) to help with chorea
Wilson’s Disease
Autosomal recessive disease that causes deposition of copper in your brain and other organs
Symptoms of Wilson’s Disease
- “Wing beating” tremor
- Keiser-fleischer rings
Tourette’s Syndrome
Autosomal dominant neurodevelopmental disorder with onset in childhood, characterized by multiple motor tics and at least one vocal (phonic) tic
Treatment for Tourette’s
- 1st: CBT
- 2nd: Clonidine (alpha agonist)
- 3rd: Tetrabenazine (monoamine depletor)
Dystonia
Neurological movement disorder syndrome in which sustained or repetitive muscle contractions result in twisting and repetitive movements or abnormal fixed postures
Treatment for Dystonia
- Levodopa
- Botox
Narcolepsy
- Patient goes from being awake to being straight into REM sleep
- Often have daytime sleepiness
- Can be triggered by emotion: Cataplexy
Investigations for Narcolepsy
- Overnight polysomnography
- Multiple Sleep Latency Test
Treatment for Narcolepsy
- Modafinil- stimulant
- SSRIs for cataplexy
Two classifications of strokes
- Ischaemic (85%)
- Haemorrhagic (15%)
Ischaemic strokes
- Artheroembolic: Arterial (white thrombus)
- Cardioembolic: Venous (red thrombus)
Haemorrhagic strokes
Due to:
- HTN
- Abnormalities (e.g. aneurysm)
- Cerebral amyloid angiopathy
- Warfarin etc
Which score do you use on A&E admission to distinguish between a stroke and a stroke mimic
Rosier score
>0 = Stroke
4 types of strokes
- Total Anterior Circulation Stroke (TACS)
- Partial Anterior Circulation Stroke (PACS)
- Lacunar Anterior Circulation Stroke (LACS)
- Posterior Circulation Stroke (POCS)
Oxford Stroke Classification has 3 criteria
- Unilateral motor loss and/or sensory loss of face/ arm/ leg
- Homonymous hemianopia
- Higher cognitive dysfunction (e.g. dysphagia)
TACS affects
Anterior and middle cerebral arteries
TACS presents with
3/3 from Oxford’s Stroke Classification (OSC)
PACS involves
Smaller arteries of anterior and middle cerebral circulation
PACS presents with
2/3 features of OSC
LACS involves
Arteries around the internal capsule, thalamus and basal ganglia
LACS presents with
- Unilateral weakness/sensory loss in face/arms/legs
- Pure sensory stroke
- Ataxic hemiparesis
POCS involves
Vertebrobasilar arteries
POCs presents with
- Isolated homonymous hemianopia
- Cerebellar/Brainstem syndromes (CNs)
- Loss of consciousness
- Decrease in consciousness
- Vomiting/Nausea
- Headaches
- Seizures
are more common in haemorrhagic strokes
Treatment for Ischaemic Stroke
<4.5 hours since onset of symptoms and haemorrhage is excluded:
- Thrombolysis: Alteplase + Aspirin (300mg)
>4.5 hours since onset of symptoms
- Surgical removal of clot
Alteplase is a
Tissue plasminogen activator
Prophylaxis treatment commenced post ischaemic stroke
A: Antiplatelets (Aspirin)
B: Blood pressure control (amlodipine if >65, ACE i if <65)
C: Cholesterol management (Statins) if >3.5
D: Diabetes management (if needed)
Treatment for haemorrhagic stroke
- Opiates and antiemetics for nausea and pain
- Increase fluids (IV drip) and blood (transfusion) to support brain
- Calcium channel blockers to cause vasodilation to maintain cerebral perfusion
- Neurosurgery
3 types of brain haemorrhages
- Subarachnoid
- Extradural (Epidural) Haematoma
- Subdural Haematoma
Subarachnoid Headache effects
Arteries in the circle of Willis
Often caused by a berry aneurysm
Subarachnoid haemorrhage bleeds into
the subarachnoid space and so can be seen in the eyes as a vitreous haemorrhage
Subarachnoid haemorrhage presents with
- Acute loss of consciousness
- “Thunderclap” occipital headache (extremely painful)
- Meningism: (Neck pain, Brudzinski’s sign positive)
Brudzinski’s Sign
Flexion of the knees/hips on flexion of the neck in meningism
Treatment for Subarachnoid Haemorrhage
Nimodipine (Calcium channel blocker)
Extradural (Epidural) Haematoma effects
- Middle meningeal artery (often due to pterion fracture in head trauma)
- Tear in the dura
“MMA fighters get head trauma”
Extradural (Epidural) Haematoma can cause a
Contra-coup injury
(Injury on the contralateral side of primary injury)
Extradural Haematoma appear as
Unilateral hyperdense biconvex lesions on CT
Extradural Haematoma Present with
- Trauma (e.g. sports head injury”
- Lucid interval followed by loss in consciousness
Subdural Haematoma effects
Bridging veins (tear)
Venous
Subdural Haematoma appear as
Hypodense crescent-shaped haemorrhage
Subdural Haematoma present as
- Low impact trauma (e.g. elderly, alcoholic fall- due to decreased clotting factors)
- Progressive headache and confusion since trauma
Treatment for Subdural Haematoma
Burr hold drainage
Racoon Eyes (peri-ocular) bruising
Anterior Cranial Fossa Fracture
“Battle sign” mastoid bruising
Middle cranial fossa fracture
- Trouble opening jaw
- Diplopia
Zygoma fracture
- Ophthalmoplegia (weakness in eye muscles)
- Ataxia
- Confusion
Wernicke Encephalopathy
Korsakoff’s Syndrome
- Impaired memory
- Confabulation
- Confusion
- Personality changes
Wernicke Encephalopathy and Korsakoff’s Syndrome are seen in
Alcoholics (and sometimes other malnourished people)
Due to deficiency of thiamine (B1)
Broca’s area is responsible for
Production of speech
Patient’s with Broca’s aphasia
- Can’t find words to say (non-fluent)
- Have trouble producing speech
- Are aware of disability
Broca’s area is found
- Left side of brain
- More anterior than Wernicke’s area
- Inferior frontal lobe
Wernicke’s area is responsible for
Speech comprehension
Patients with Wernicke’s aphasia
- Cannot comprehend their own speech
- Cannot comprehend other people’s speech
- Are not aware of their disability
Can produce fluent sentences, however, they do not make sense
Types and causes of Headaches
- Migraine
- Trigeminal Autonomic Cephalopathies
- Cluster
- Paroxysmal Hemicrania
- SUNCTs
- Tension
- Sinusitis
- Idiopathic Intracranial Hypertension (IIH)
- Temporal Arteritis
- Trigeminal Neuralgia
- Acute Glaucoma
Headache Red Flags
- New onset >55
- Previous Malignancy
- Immunosuppressed
- Early morning (wakes them up)
- Exacerbation by valsalva maneouvre
IHS Criteria for a Migraine
2/3 of:
- Debilitating
- Unilateral
- Throbbing
+ nausea/ photophobia/ phonophobia
+ aura
Migraine’s usually last for
4-72hrs
You only treat migraines if they are happening
3 times per month
Acute Migraine treatment
- During aura (pre-pain): Triptan
- During pain: NSAID and antiemetic
Migraine prophylaxis
- Propranolol
- Topiramate
- Amitriptyline
Trigeminal Autonomic Cepholopathies (TACs) consist of
- Cluster
- Paroxysmal Hemicrania
- SUNCTs
Cluster headaches last for
45-90mins
Cluster headaches presentation
- 30 year old
- Unilateral supraorbital pain
- 1-8 headaches per day for many weeks
Acute treatment of cluster headache
- High flow O2
- Steroids
- Triptans
Prophylaxis for Cluster headaches
Verapamil (Calcium channel blocker)
Paroxysmal Hemicranias last for
2-30mins
Presentation of Paroxysmal Hemicrania
- Elderly patient
- Severe unilateral pain
- 1-40 headaches per day
- Horner’s Syndrome
Treatment for Paroxysmal Hemicrania
Indomethacin
SUNCT stands for
- Short-lived
- Unilateral
- Neuralgiform
- Conjunctival infection
- Tearing
Treatment for SUNCTs
Antiepileptics
- Lamotrigine
- Gabapentin
Tension headaches last for
30mins - 7 days
Presentation of a tension headache
- Tight band
- Non-pulsatile
- Stressed patient
Treatment for Tension headache
- Antidepressant for 3 months
- Stress relief
Presentation of a sinus headache
- Recent viral infection
- Worse when leaning forward
Presentation of Idiopathic Intracranial Hypertension
- Young and overweight patients
- Increased CSF (papilloedema)
- Morning vomiting/ nausea
Treatment for Idiopathic Intracranial Hypertension
- Lose weight
- Acetazolamide
- Ventricular shunt
Side effects of ventricular shunts
Can cause infection
Can cause low-pressure headache
Trigeminal Neuralgia Presentation
- Female patient in 60s
- V2/V3 pain on touching
- Gone in seconds
Treatment for Trigeminal neuralgia
- Gabapentin
- Carbamazepine
- Pregabalin
Temporal arteritis presentation
- Temple pain
- Scalp tenderness
- Associated with jaw claudication
Investigation for Temporal arteritis
Temporal artery biopsy
Treatment for Temporal arteritis
Steroids
Acute Primary Angle Closure Glaucoma Presentation
- Severe eye pain
- Vomiting and nausea
- Blurred vision
- See’s lights around halos
- Tearing
Treatment for Acute angle closure glaucoma
- Admit to hospital
- Pilocarpine eye drops
- Acetazolamide
- Pain relief
3 Types of Meningitis
- Bacterial
- Viral
- Fungal
Most common type of meningitis
Viral
Presentation of Meningitis
- Meningism
- Fever
- Rash (non-blanching purpuric)
- Headache
- Photophobia
- Decreased GCS
Organisms that affect Neonates
- Listeria
- Group B Strep
- E. coli
Organism that affect children
H. Influenzae
Organism that affect teens (10-21)
- Neisseria Meningitidis
Organisms that affect adult population (21+)
- Strep pneumoniae
- Neisseria meningitidis
Organisms that affect elderly >65
- Listeria
- Strep pneumoniae
Gram-positive bacillus found in deli foods
Listeria
Gram-negative bacillus
H Influenzae
Gram-positive cocci found in nasopharynx
Strep pneumoniae
Most common cause of bacterial meningitis (51%)
Gram-negative cocci, found intracellularly
Neisseria Meningitidis
Second most common cause of bacterial meningitis (37%)
Most likely organisms to cause meningitis due to a head fracture
- Staph aureus (gram-positive cocci)
- H influenza
Most likely organisms to cause bacterial meningitis due to a cribriform plate fracture
- Strep pneumoniae
- H influenza
Most likely organism to cause bacterial meningitis from a CSF shunt
Staph epidermidis
Viral meningitis is usually caused by
Enterovirus (Echovirus)
Common in Autumn
Fungal meningitis is most usually caused by
Cryptococcal neoformans
Common in immunosuppressed people
Investigations for Meningitis
LP
(Don’t do if increased CSF pressure)
Bacterial meningitis will show
- High WBC (neutrophils)
- High protein
- Low glucose
- High opening pressure
- Cloudy CSF
Viral meningitis will show
- High WBC (lymphocytes)
- Normal protein
- Normal glucose
- Clear CSF
TB meningitis will show
- High WBC (lymphocytes)
- High protein
- Low glucose
- Yellow CSF
If someone has meningitis then
notify public health within 24hrs
1st line treatment in bacterial meningitis (adults)
Dexamethasone + Ceftriaxone
“Adults do triathlons”
Give steroids to reduce inflammation from damaging bacterial debris.
Treatment for bacterial meningitis for children
Dexamethasone + Cefotaxime
“Because kids don’t pay taxes”
Treatment for listeria infection in adult/children meningitis
Normal 1st line treatment + amoxicillin
If resistant to amoxicillin: Vancomycin + rifampicin
Treatment for Penicillin Allergy Bacterial Meningitis
Dexamethasone + Chloramphenicol + Vancomycin
Treatment for Listeria Penicillin Allergy Meningitis
Normal treatment + Co-trimoxazole
Do not give steroids in meningitis in
Cases that involve
- Immunocompromised patients
- Post-surgical patients
- Septic patients
As they will make them more immunosuppressed
Treatment for Viral meningitis
Aciclovir
Treatment for Fungal Meningitis
IV Amphotericin B + Fluconazole
Normal CSF production
- 0.35ml/min
- 500ml per day
CSF is produced in
Choroid plexus
and 25% in the interstitial fluid
CSF if absorbed in
arachnoid granulations
Hydrocephalus presents with
- In neonates: Bulging fontanelle
- Nausea/vomiting (especially in morning)
- Bilateral Headache (wakes you up)
- Sunsetting of the eyes (fixed downward eyes)
- Seizure
- No aura
Treatment of Hydrocephalus
- Ventricular shunt
- Acetazolamide
Argyl-Robertson pupils
“Prostitutes sign” - as they accommodate but don’t react
Neurosyphilis
Sunsetting sign and vertical gaze palsy
Perinaud’s Syndrome
Cranial nerves that come out above the pons
CN I, II, III, IV
Cranial nerves that come out of the pons
CN V, VI, VII, VIII
Cranial nerves that come out below the pons
CN IX, X, XI, XII
3 types of brain herniation
- Subfalcine
- Transtentorial
- Tonsilar
Subfalcine Herniation
Cingulate gyrus us pushed under the falx cerebri
Transtentorial “Uncal” Herniation
Temporal lobe herniates under the edge of the tentorium cerebelli
Transtentorial herniation will cause
Blown pupil “dilated” due to CN III compression
Tonsillar Herniation
Cerebellar tonsils are forced through the foramen magnum
this is known as “coning”
Tonsilar herniation will cause
- HTN
- Bradycardia
- Respiratory arrest
- Eventually death
A primary cause for tonsillar herniation
Chiari Malformation
A secondary cause for tonsillar herniation
- SOL in brain
- Doing a LP in a patient with increased CSF
Brain pathology often presents with
Hydrocephalus symptoms
Mostly in Non-gliomas types as they are not in the brain tissue and cause mass effect
Most common brain cancer is
Metastatic (Secondary)
Metastatic brain cancer is most commons spread from the
- Lung
- Breast
- Melanoma (skin)
- Colon
- Kidneys
2 classifications of primary brain cancer
- Glioma
- Astrocytoma
- Ologodendroglioma
- Non-Glioma
- Meningiomas
- Pituitary
- Schwannomas
- Pineal gland tumours
Gliomas in kids occur
Infratentorial
Gliomas in adults occur
Supratentorial
Astrocytomas occur
at any age
Astrocytoma grade I
Local benign lesion
Vomiting and reduced appetite
- Pilocytic in kids (optic gliomas)
- Pleomorphic xanthoastroma in children-teens
Tx: Surgical removal
Optic gliomas are associated with
Neurofibromatosis Type 1
Astrocytoma grade II
Low grade, pre-malignant
Frontal, temporal and parietal
- Fibrillary (firm consistency)
Tx: Chemo/radiation + surgery
Astrocytoma Grade III
Anaplastic astrocytoma
2 years prognosis
Astrocytoma Type IV
Glioblastoma Multiforme
“Patchy enhancement”
1 year prognosis
Tx: Surgery + radiotherapy + temozolomide (MGMT+)
Oligodendroglial tumours occur in
Middle-aged adults
- Calcifications on MRI “toothpaste like”
- Frontal lobe involvement
- Seizures
Oligodendroglial
Treatment for Oligodendroglial tumours
- Radio
- Chemo
Meningiomas occur in
>40s
Types of Meningiomas
CCRAP
C: Clear cell
C: Choroid
R: Rhabdoid
A: Atypical
P: Pupillary
Meningiomas
- Dural tail
- Often due to previous radiation
- Blush effect on angiography
- Increased bone lesions around the area
In subtypes can be :
- Meningioma en plaque (Carpet sheet-like lesion, infiltration of dura and bone)
Tx: Surgery
Pituitary Tumours
Cause:
- Cushing’s syndrome
- Bitemporal hemianopia
Prolactinoma: increased prolactin
Schwannoma
Acoustic neuroma:
- Hearing loss
- Vertigo
- Tinnitus
others affect: CN V, VII, VIII
3 main types of pineal gland tumour
- Choriocarcinoma
- Yolk sac
- Germinoma
Increased B-hCG pineal gland tumour
Choriocarcinoma
Increased AFP Pineal tumour
Yolk sac (massively raised)
Teratoma
Increased PLAP Pineal tumour
Placental Alkaline Phosphotase
Germinoma
Symptoms of Pineal tumours
- Commonly obstruct CSF flow and cause non-communicating hydrocephalus
- Vertical gaze palsy (CN IV)
Chemo treatment for Brain tumours
“PCV”
Procarbazine, CCNU (Lomustine), Vincristine
Schwann cells produce myelin in
PNS
Oligodendrocytes produce myelin in the
CNS
Astrocytes make up the
Blood brain barrier
Ependymal cells are responsible for
CSF regulation
Microglia are
Phagocytes
Alpha/Beta/Delta receptors are
- Thinly myelinated
- Sharp pain= first response
C fibres are
- Not myelinated
- Throbbing pain= secondary response
A-Alpha receptors
Proprioception
A-beta
Mechanoreceptors
A-delta
Pain (nociceptors) and temperature
Types of mechanoreceptors
- Meissner’s corpuscles
- Merkel discs
- Ruffini endings
- Pacinian corpuscles
Meissner’s corpuscles
Light touch
Merkel discs
Pressure
Ruffini endings
Stretch sensation
Pacinian corpuscle
Vibration
Lateral geniculate nucleus
Optic fields
Medial geniculate nucleus
Auditory
