12.1 Flashcards
List modifiable risk factors for stroke.
- Obesity
- Hypertension
- Diabetes (increases risk by 2-4 times)
- AF-
Hypertension
What is the target BP?
<130/80
What is the tentorium?
A structure which separates the 2 hemispheres of the brain from brainstem and cerebellum
What type of bleed is a subdural haematoma?
Venous
What type of bleed is a extradural haematoma?
Arterial
What is clinical response to brain injury?
- Altered consciousness levels
- Dizziness
- Pain
- Vomiting
- Retrograde amnesia
What is the effect of secondary injury?
- Ischaemic = ruptured spleen can cause lessened perfusion to brain
- Infection = fracture to skull could lead to meningitis
- Seizures = use up a lot of brain substrate
How is cerebral blood flow autoregulated?
Vasodilation and vasoconstriction
What is an uncal herniation?
Transtentorial downward brain herniation
Define stroke.
Sudden focal neurological deficit due to vascular lesion lasting longer than 24hrs.
Define TIA.
Focal deficit lasting a few seconds to 24hrs with complete clinical recovery
What are the 4 arteries which run to the brain?
- 2 vertebral arteries
- 2 internal carotids
20% of strokes are what?
80% of stroke are what?
Haemorrhagic 20%
Ischaemic 80%
ICD-10 definition of dementia
o A syndrome due to disease of brain
o Usually of a chronic or progressive nature
o Disturbance of multiple higher cortical functions
o Consciousness is not clouded – this distinguishes dementia from delirium
o Cognitive impairments are commonly accompanied by deterioration in emotional control, social behaviour, motivation o Impairment sufficient to impact on activities of daily living (ADLs)
Anterior spinothalamic tract
Crude touch
Lateral spinothalamic tract
Pain + temperature
What is dementia?
Syndrome due to disease of the brain, usually chronic or progressive.
What are the different types of dementias?
- Alzheimer’s - most common
- Vascular dementia
- Mixed dementia - Alzheimers and vascular dementia
- Lewy-body dementia
- Fronto-temporal dementia
- Others e.g. Parkinson’s disease with dementia
Differential diagnosis of dementia.
- Ageing
- Mild cognitive impairment
- Depression
- Delirium
- Physical health problem e.g. thyroid
Features of Alzheimer’s
- Insidious onset with gradual progression
- Memory loss
- Language impairment
- Decline in motor skills and ADL
- Loss of recognition skills
- Disorientation
What is the normal role of tau protein?
Allows messaging between cells
What is the normal role of amyloid?
Protects against calcium influx and glutamate excite-toxicity
- Drugs used in Alzheimer’s
1) AChesterase inhibitors. used in mild-moderate AD (e.g. donepezil, galantamine, rivastigmine)
2) NMDA receptor antagonists, to reduce glutamate, used in moderate-severe AD (e.g. memantine)
What is vascular dementia?
Dementia due to problems with blood supply to the brain - posterior circulation
Risk factors include hypertension, high cholesterol, diabetes, smoking, IHD
Difference between dementia with lewy bodies and parkinsons disease with dementia.
Dementia with lewy bodies = early cognitive symptoms, rapidly progressing dementia, fluctuation, hallucination,
Parkinsons disease with dementia = motor symptoms for more than a year, apathy, slowing of thought and executive functioning
Which feature is prominent early on in dementia with Lewy bodies?
Visual hallucinations
Fuctuations in cognition/performance, visual hallucinations, parkinsonism
Which brainstem area is degenerated in dementia with Lewy Bodies?
Substantia nigra - involved in dopamine production
Features of fronto-temporal dementia
- Mainly early onset- 10% familial
- Mutation in tau protein
3 main syndromes of fronto-temporal dementia.
- Dementia of frontal type - presents with emotional/behavioural change rather than STM loss
- Progressive non-fluent aphasia - progressive difficulty with words
- Semantic dementia - loss of knowledge of meaning of words
Result of a lesion in the right internal capsule or motor cortex.
Contralateral upper motor neuron weakness
Result of a lesion in the right cranial nerve nuclei.
Ipsilateral lower motor neuron weakness
Motor result of a lesion on the right side of the spinal cord.
Ipsilateral upper motor neuron weakness
Lesion in the parietal cortex
Contralateral sensory deficit
Sensory result of a lesion on left side of spinal cord.
Contralateral spinothalamic loss - pain, temp
Ipsilateral dorsal column loss - fine touch, vibration, proprioception
Are motor structures represented medially or laterally in the nervous system.
Medially (sensory are lateral)
Lesion in substantia nigra
Parkinsonian features
Lesion in red nucleus
Cerebellar like features
Role of vestibulocerebellum (Flocculonodular lobe anatomically)
Balance, posture, eye movements
Role of spinocerebellum (vermis and paravermis anatomically)
Postural control
The spinocerebellum contains sensory maps as it receives data on the position of various body parts in space: in particular, the vermis receives fibres from the trunk and proximal portions of limbs.
While the intermediate parts of the hemispheres receive fibres from the distal portions of limbs.
The spinocerebellum is able to elaborate proprioceptive input in order to anticipate the future position of a body part during the course of a movement, in a “feed forward” manner.
Role of cerebrocerebellum (lateral parts of hemispheres).
Fine co-ordination with planning of limb movements about to occur
Features of cerebellar dysfunction.
V - vertigo A - ataxia N - nystagmus I - intention tremor S - slurred, staccato + scanning speech H - hypotonia D - dysmetria, dysdiadokinesia
IPSILATERAL LIMB SIGNS
Lateral rectus eye muscle supplied by what?
Abducens (CN6)
Superior oblique eye muscle supplied by what?
Trochlear (CN4)
Complete oculomotor nerve lesion.
- Eye down and out
- Pupil dilated
- Partial ptosis from paresis of levator palpebrae superioris
Horners syndrome
- Smaller pupil
- Cluster headache
- C8/T1 pathology
- Ptosis
- Anhydrosis
Upper motor neuron lesion signs
Muscle wasting +
Increased tone
Increased reflexes
Decreased power
Spastic posturing
Lower motor neuron lesion signs.
Muscle wasting ++
Fasiculations
Decreased tone
Decreased reflexes
Decreased power
Hyoglossal nerve palsy
- Tongue deviates to side of weakness
- Unilateral in LMNL
- Contralateral in UMNL
UMNL flexors
Stronger than extensors - this is why in cerebral palsy hand is flexed in front
When are fasciculation’s present?
When there is a problem with the anterior horn cell LMN
Increased tone - spastic
Increased tone - rigid
Spastic: Initially stiff but it gets easier
Rigis: Constant stiffness - parkinsonian syndromes
Decorticate positioning.
CORTICAL LESION
- Adduction stronger than abduction
- Abnormal flexion
- Foot plantar flexed
Decerebrate positioning
- Arms extended
- Damage to upper brainstem
- Wrists pronated
Plantar response
- Up going big toe = pathology (hence positive Babinski’s sign)
- Positive test indicates UMNL or normal in new born
Supinator reflex
C5 C6
Biceps reflex
C5 C6
Triceps reflex
C6 C7
Ankle reflex
S1 S2
Knee reflex
L3 L4
Central cord lesion e.g. syringomyelia
Tube within spinal cord
Dissociative sensory loss - dorsal columns not affected
UMN signs below level if pressure on corticospinal tracts
Anterior spinal artery syndrome
Anterior 1/3rd of spinal cord supplied by anterior spinal cord
- If anterior artery occluded, people end up with total paralysis below the level
- Complete bilateral motor loss below the level
- Preservation of sensation carried by dorsal columns
- Bilateral loss of spinothalamic function below
Romberg’s test
- Patient stands with feet together + ask them to close their eyes
- If they wobble there is a problem with vestibular system
Virchow’s triad
Virchow’s triad or the triad of Virchow describes the three broad categories of factors that are thought to contribute to thrombosis.
- Blood vessel wall
- Blood flow
- Blood constituents - too many red cells or too many platelets = clot, not enough clotting factors = bleed
- endothelial injury
- hypercoagulability
- stasis of blood flow
Sites of brain haemorrhage (Intracerebral)
Subarachnoid - arterial
Subdural - venous
Extradural - arterial
Intracerebral haemorrhage causes
- Rupture of aneurysm
- Arteriovenous malformation
- Cavernoma
- Bleed into infarct
- Bleed into tumour
- Trauma
Define sedation
Allows patient to tolerate unpleasant diagnostic or surgical procedures - verbal contact can be maintained
Define coma
State of extreme unresponsiveness where there is no voluntary movement or behaviour
Define anaesthesia
If GA then drug induced and predictably reversible coma
Classes of anaesthetic agents
GA
IV or inhaled Local - esters and amides
Neuromuscular blocking agents - depolarising/non-polarising
Analgesia - opioids
How do GA work?
Act on GABA, glutamate and other NMDA receptors
- Volatile act on alpha and beta subunits or GABA.
- Intravenous act on beta subunit of GABA.
Principal effects of anaesthesia
Unconsciousness - can still feel pain but can’t form memories
Loss of reflexes
Analgesia
Difference between onset of volatile and IV GA
Rapid onset for IV.
Slow onset for volatile.
Examples of volatile GA
NO, isoflurane, sevoflurane
Examples of intravenous GA
Propofol, ketamine, thiopentone
Side effects of GA?
Cardiac suppression and respiratory depression
MOA of local anaesthetic
- Block voltage sensitive Na+ channels
- Pain still sensed by nociceptors but transmission to brain and spinal cord is inhibited
Effect depends on:
- Diffusion gradient
- Fibre size
- Myelination
A fibres
There are 4 subdivisions: alpha (ɑ), beta (β), gamma (ɣ), and delta (δ).
A-alpha:
- Large diameter (13-20μm)
- Myelinated
- Proprioception
- Include type Ia (muscle spinle) and Ib (golgi tendon) sensory fibres of the alternative classification system
A-beta:
- Smaller diameter (6-12μm)
- Myelinated
- Touch
A-gamma:
- Smaller diameter (5μm)
- Type of LMN invoved in muscle contraction
- Role = keeping muscle spindles taut, thereby allowing the continued firing of alpha neurons, leading to muscle contraction
A-delta:
- Smaller diameter diameter (1-5μm)
- Myelinated
- Pain and temperature
B fibres
Group B nerve fibers are axons, which are moderately myelinated, which means less myelinated than group A nerve fibers, and more myelinated than group C nerve fibers.
Their conduction velocity is 3 to 14 m/s.
They are usually general visceral afferent fibers and preganglionic nerve fibers of the ANS
C fibres
- Small diameter (0.2-1.5μm)
- Unmyelinated,
- Low conduction velocity
- Pain, temperature, itch
They include postganglionic fibers in the ANS for vasodilation, and nerve fibers at the dorsal roots (IV fiber). These fibers carry sensory information.
Neuromuscular blocking drugs - antagonists
- Non-depolarising
- Competitive
- E.g. tubocurarine + atracurium
Muscle relaxation in surgery
Neuromuscular blocking drugs - agonists
- Depolarising
- Non-competitive
- Acts on nicotinic receptors
- E.g. suxamethonium
Muscle paralysis
Are nicotinic receptors mostly post-synaptic or pre-synaptic?
Pre-synaptic
MOA of suxamethonium (aka succinylcholine)
Binds to ACh receptors which causes depolarisation of muscles
MoA: “persistent” depolarization of the neuromuscular junction. This depolarization is caused by Succinylcholine mimicking the effect of acetylcholine but without being rapidly hydrolysed by acetylcholinesterase. This depolarization leads to desensitization.
4 stages of anaesthesia
- Induction - initial administration to loss of consciousness
- Excitement - excited and delirious activity - RR + HR may become irregular
- Surgical anaesthesia - skeletal muscles relax
- Overdose - too much medication relative to amount of surgery resulting in severe brainstem or medullary depression
Reliable clinical signs of anaesthesia.
Muscle tone - jaw
Light reflex
Eyelid reflex
Lacrimation
Balance
Term used to describe the dynamics of body posture to prevent falling
Centre of Mass
Weighted average of CoM of each body segment in 3D space
Centre of Gravity
Vertical projection of COM onto ground
Postural control
Keeping body’s CoG over during quiet stance and within Base of Support (BoS) during active movements
Stretch (myotatic) reflex
- Muscle spindles lengthen in response to postural control
- Signalled by afferent nerve fibres
- Connect directly to motor neurons
- Activates that same muscle
Monosynaptic reflex
Afferents connect directly to efferents without interneurons
Ankle strategy
- In response to small, slower disturbances
- Shifts CoG about ankle joint
- Used on surfaces with low resistance to shear forces
Hip strategy
- In response to larger, faster disturbances
- Shifts CoG about hip joint by flexion/extension
Stepping strategy
- In response to largest, fastest disturbances
Sensory components of balance
Somatosensory - skin receptors
Proprioceptive - muscle spindles + golgi tendon organs
Visual - eyes
Vestibular - inner ear
Lesion at optic chiasm
Lose lateral part of left and right eye (hemianopia)
Where does light enter the eye?
Cornea
Glaucoma
Damage to the optic nerve due to an overproduction of aqueous humour, in which the trabecular meshwork cannot keep up with drainage of.
Causes an increase in pressure which pushes the optic nerve into the cavity in the back of the eye, causing damage to the axons
Fovea
Region of highest resolution vision
Structure of retina
3 basic layers:
- Outer ganglion layer
- Middle layer of amacrine and bipolar cells
- Bottom layer of photoreceptors (rods + cones)
Rods
Black and white.
Night conditions
Cones
Colour Daytime vision
Role of horizontal and amacrine cells
Integrate information laterally - allow communication horizontally between cells
3 different cone types
Long wavelength (L) cones - red, orange, yellow
Middle wavelength (M) cones - green
Short wavelength (S) cones - blue - not X linked recessive like the 2 above but instead is on chromosome 7
Choroid
Dense network of vasculature
o Connective tissue + dense vascular network that provides nutrients to outer surface retina
o Choroid receives its blood supply from central retinal artery (that emerges from back of eye)
o Retinal arteries + veins supply the inner surface of retina is (come in through optic nerve fasciculus)
o Choroid provides all eye layers w/ 90% of their blood supply
Dichromat
Only have 2 different cone types
Protanopia
Lack L cones - red
Deuteranopia
Lack M cones - green
Tritanopia
Lack S cones - blue
Protanomalous trichomat
Weak L cone
o Weak red cones, they shift their sensitivity to higher wavelength (more sensitive to green) making it difficult to distinguish between red + green
Deuteranomalous trichomat
Weak M cone
o Weak green cones, they shift their sensitivity to lower wavelength (more sensitive to red) making it difficult to distinguish between red + green
Tritanomalous trichomat
Weak S cone
o Weak blue cones
Test for colour blinded
Ishihara plate
Visual receptive field
All of the photoreceptors that feed in information to that bipolar cell
How many layers of Lateral geniculate nucleus?
The lateral geniculate nucleus is a sensory relay nucleus in the thalamus of the brain
SIx.
It has multiple layers:
4 sets of ‘parvocellular layers’ – Small cells
2 sets of ‘magnocellular layers’ – Large cells
o Each layer receives input from a different eye (contralateral or ipsilateral), information from each eye is kept separate
How many parvocellular layers and which ones are they?
Four.
3, 4, 5, 6
Small cells, top 4 layers
Receive input from B (midget) ganglion cells – smaller
Separate information from the 3 cone types
Most of these cells (90%) have colour-opponent receptive fields (sensitive to different colour lights)
• Can use these layers to discriminate different colours
Lesion – impairs colour vision, visual acuity, fine stereopsis, texture discrimination, doesn’t affect speed/motion discrimination
How many magnocellular layers and which ones are they?
Two.
1, 2
Large cells, bottom 2 layer
Receive input from A (parasol) ganglion cells – larger
Combine info from all 3 cone types so sensitive to black and white vision (changes in brightness)
Lesion – impairs ability to discriminate movement, doesn’t affect colour vision or visual acuity
Magnocellular
Receives information from A (parasol) ganglion cells which combine information from all 3 cones.
Sensitive to black and white and changes in brightness.
Parvocellular
Receives information from B (midget) ganglion cells - separates the 3 cone types
Able to differentiate colour
Magnocellular lesion
- Impaired ability to discriminate movement
- Impairs low spatial frequency (coarse, blurry patterns)
- Doesn’t affect colour vision
- Doesn’t affect visual acuity
Parvocellular lesion
- Impaired colour vision
- Impaired visual acuity
- Impaired fine stereopsis (depth, 3D vision)
- Impaired texture discrimination
- Doesn’t affect speed discrimination
P (parvo) stream
- Prefers high spatial frequencies
- Prefers slow movement
- Is colour selective
- Essential for texture discrimination
- Essential for fine stereopsis
M (magno) stream
- Prefers low spatial frequencies
- Essential for fast flicker and motion detection
- No colour selectivity
How many layers does the striate (primary visual cortex) have?
6
Where do the magno and parvocellular streams project into?
Different areas of layer 4 of the striate cortex
What do the koniocellular cells carry?
Information from S cells
Where do the koniocellular cells project to?
Layers 2 and 3
Ocular dominance
Vertical stretch of striate cortex that responds primarily to information from 1 eye
Where is centre of visual field processed?
Very back of brain
Where is peripheral vision processed?
Anterior of occipital lobe
Specialisation of extrastriate areas
V2 - unknown
V3 - depth perception and visual acuity
V4 - colour
V5 - motion
Which higher level visual area recognises faces?
Fusiform face area
Which higher level visual area recognises scenes?
Parahippocampal place area
Which higher level visual area recognises objects?
Lateral occipital cortex
Where pathway
Parvocellular route to V1 –> dorsal route to V5 –> posterior parietal cortex
What pathway
Magnocellular route to V1 –> ventral route to V4 –> infers-temporal cortex
Striate cortex lesion
At least partially blind but still able to navigate
Blindsight pathway
Retina –> superior colliculus –> pulvinar –> posterior parietal cortex
Balint-Holmes syndrome
Impairment in using visual information to guide motor movements
What is the ‘what pathway’ also known as?
The ventral stream
What is the ‘where pathway’ also known as?
The dorsal stream
What is the dorsal stream involved in?
Processing the object’s spatial location relative to the viewer and with speech repetition
What is the what pathway involved with?
Object and visual identification and recognition
Describe visual form agnosia
Unable to recognise objects
How many cranial nerves?
24 (12 pairs)
Cerebral nuclei-cranial openings
I, II
Midbrain nuclei-cranial openings
III, IV
Pontine nuclei-cranial openings
V, VI, VII, VIII
Medullary nuclei-cranial openings
IX, X, XI, XII
Eye movement CNs
III, IV, VI
Special sensory CNs
I, II, VIII
Parasympathetic CNs
II, VII, IX, X
Olfactory nerve - CN I
Pathway: Olfactory epithelium in superior nasal mucosa –> perforations in cribriform plate –> mitral cells of olfactory bulb –> olfactory tract - secondary neurons –> primary olfactory cortex + amygdala
No thalamic precortical relay - doesn’t run through thalamus
Test - can you smell? Unilateral ansomia - fracture/meningioma Bilateral anosmia - cold/viral infection
Optic nerve - CN II
Enters skull through optic canal with ophthalmic artery and projects to LGN. From LGN you get optic radiations to the primary visual cortex in occipital lobe
Test - confrontational visual field, pupillary response + visual acuity (snellen)
Light goes in through optic nerve and then pupil constriction caused by oculomotor nerve
Oculomotor nerve - CN III
2 nuclei in midbrain 1. Oculomotor nuclei - motor 2. Edinger-Westphal - PS
Runs through cavernous sinus and exits through superior orbital fissure PS nerve fibres on outside of nerve
Space occupying lesion = dilated pupil - you would get this before muscle paralysis
PS constricts pupil - runs to sphincter papillae and ciliary muscle
Test with trochlea and abducens
SUPPLIES MEDIAL RECTUS = ADDUCTS
Trochlear - CN IV
Comes out of back of midbrain inferior to inferior colliculus before running around the side of the midbrain and exiting via the cavernous sinus + superior orbital fissure and runs to superior oblique muscle.
Turns eye down + out
Only CN to exit brainstem on dorsal surface
Abducens - CN VI
Exits brainstem at pontine medullary junction. Runs through cavernous sinus and exits via the superior orbital fissure.
Supplies lateral rectus.
Black tract = main central connection of oculomotor, trochlea and abducens
SUPPLIES LATERAL RECTUS = ABDUCTS
List the eye movements each eye muscle is responsible for.
Superior oblique - depresses, abducts and medial rotation
Inferior oblique - elevate, abduct and lateral rotation
Superior rectus - elevate, adduct and medial rotation
Inferior rectus - depresses, adducts and lateral rotation
Medial rectus - adduction
Lateral rectus - abduction
Which extraocular muslce is innervated by the trochlear nerve?
Superior oblique muscle
Mnemonic for simplified actions of the eye muscles:
- Obliques Abduct whereas Rectii Adduct (except LR)
- Superiors Intort whereas Inferior Extort
- Rectii act according to their names whereas Obliques act opposite to their names
Which extraocular muscles are innervated by the oculomotor nerve (CNIII)?
- Superior rectus
- Inferior rectus
- Medial rectus
- Inferior oblique
Levator palpebrae superioris
What is the function of the levator palpebrae superioris muscle?
Elevates + Retracts upper eyelid
Which extraocular muscles does the abducens nerve innervate?
- Lateral rectus
- Retractor bulbi
Pupillary light reflex
- Light comes in via optic chiasm
- Runs to LGN but bypasses it and synapses at pre-tectal nucleus
- After pre-tectal nucleus, transmits bilaterally to oculomotor nucleus
- From oculomotor nucleus runs to ciliary ganglion and constrictor pupillae
Trigeminal nerve - V
- Ophthalmic - runs in cavernous sinus and exits through superior orbital fissure. Sensory.
- Maxillary - exits skull through foramen rotandum. Sensory.
- Mandibular - exits skull through foramen oval.
Mixed nerve.
Exits via side of pons and forms ganglion which sits in middle cranial fossa
Test - corneal reflex, sensation of face, palpate masster and temporalis, jaw jerk
Facial - VII
Mixed nerve - exits at pontine medullary junction
Runs into internal auditory meatus with vestibulocochlear + intermediate nerve with special sensory fibres.
Some PS fibres from superior salivatory nucleus which are distributed to:
Nasal glands
Palatine and lacrimal glands
Submandibular and sublingual glands
Special sensory from anterior 2/3rds of tongue run up chorda tympani over handle of malleus and synapses and geniculate ganglion.
Testing - facial expression
Ramsey-Hunt syndrome
Varicella zoster of facial nerve
Vestibulocochlear - VIII
Cochlear and vestibular nerve which run together
Exits at pontine-medullary junction
Enters skull through internal auditory meatus and is distributed to structures within the ear
Test - Rinne and Weber
Glossopharyngeal - IX
Medullary - PS + motor
Exits skull at jugular foramen with vagus and spinal accessory nerve + runs to parotid, carotid body and pharynx
Test - gag reflex
Vagus - X
Medulla
Comes out of brainstem inferior to rootlet of glossopharyngeal.
Exits skull through jugular foramen.
Branch to muscles of larynx, pharynx, thorax and abdomen.
Test - say ahhh (this is with cranial accessory nerve) - uvula points to normal side
Accessory - XI
Cranial and spinal segments
Spinal from upper 3 cervical segments and runs through foramen magnum into cranium.
Exits through jugular foramen.
Supplies sternocleidomastoid and trapezius
Test - turn head against resistance and shrug shoulders
Hypoglossal - XII
Medulla
Exits brainstem between pyramid and olive of medulla.
Runs through hypoglossal canal into the area just inferior to the angle of the mandible.
Supplies intrinsic muscles of the tongue
Test - stick tongue out (tongue points to side of lesion)
Define seizure
An abnormal paroxysmal discharge of neurons sufficient enough to cause clinically detectable intermittent disturbance of consciousness, behaviour, motor and sensory function
Define status epilepticus
Status epilepticus is a single epileptic seizure lasting more than five minutes or two or more seizures within a five-minute period without the person returning to normal between them.
Partial complex seizures
Loss of consciousness.
No loss of postural control.
Affects only a single brain lobe
But individual loses awareness (becomes dazed)
Individual gets an aura (odd taste/smell) before becoming dazed (doesn’t lose consciousness)
Simple complex seizures
No loss of consciousness.
Seizure in frontal lobe:
• May affect motor cortex
• Symptoms may just be contralateral muscles twitching w/ full consciousness + awareness
Seizure in temporal lobe:
• May just cause off taste in mouth for few seconds
3 types of seizures?
1) Generalised - tonic/clonic, absence, myoclonic, atonic. Note causes complete LoC.
2) Focal/partial - simple partial (no loss of consciousness), complex partial (loss of con)
3) Focal with secondary generalisation - seizure starts in 1 lobe but then spreads to all brain
Tonic-clonic seizure
GRAND MAL
Type of generalised seizure that affects the entire brain
Causes convulsions (alternate contractions/extension of muscles)
Loss of consciousness + there is a postictal phase
- Electrical discharge starts at centre then spreads to cerebral cortex
- Sudden loss of consciousness follow by tonic phase
- body is stiff, breathing stops (may be cyanotic)
- Clonic phase: rhythmical shaking, may bite tongue, eyes roll back, loss of bowel or bladder control
Absence seizure
Patient suddenly stares vacantly
May be myoclonic jerks
Individual appears ‘absent’ for a while + may or may not have postictal disorientation
Brief loss + return of consciousness, generally not followed by a period of lethargy
Define epilepsy
A condition where seizures recur, usually spontaneously
Seizures only happen in cerebral cortex (doesn’t happen in. cerebellum, brainstem)
Atonic seizure
Sudden loss of tone of postural muscles causes patient to fall
Involves loss of muscle tone for >1 second, individual may collapse
Also called drop seizures, akinetic seizures or drop attacks
Brief lapse in muscle tone that are caused by temporary alterations in brain function
The seizures are brief – usually less than 15 seconds
Frontal lobe - normal role
o Intellectual function
o Inhibition
o Bladder continence
o Saccadic eye movement – in seizures, eyes move opposed the side of lesion
o Motor function
o Expression of language – seizure may cause inability to speak
Frontal lobe seizures
o Jacksonian seizures – one sided o Adversive seizures o Todd’s paresis – paralysis of one side o Very brief + often nocturnal o Hyperkinetic behaviour, vocalisation o Retained consciousness o ASNFLE – genetic o EEG can be normal because the frontal lobe is so large
Parietal lobe - normal role
o Sensory integration
o Receptive language function
Parietal lobe seizures
o Positive sensory disturbance (paraesthesia)
o Motor activity in affected body parts follows in 50% of cases
o D/D TIA, migraine
Temporal lobe - normal role
- Memory - Smell - Hearing - Emotion - Vestibular
o Memory – seizures may cause memory hallucinations (déjà vu)
o Smell – seizures may cause olfactory hallucinations (weird smell that doesn’t exist)
o Hearing – seizure may cause auditory hallucination (hearing sound that doesn’t exist)
o Vestibular – seizure may cause vestibular hallucinations (feeling of falling/moving/vertigo)
o Emotion – seizure may cause emotional disturbance
Temporal lobe seizures
o Gradual evolution over 2-3 minutes, lasts 2-5 minutes
o Aura – epigastric, smell, taste, déjà vu, fear
o Auditory/visual hallucinations
o Pallor, flushing, changes in heart rate
o Speech arrest or repetitive vocalisation
o Motionless stares
o Automatism – lip smacking, fidgeting, fumbling (odd behaviours)
o Postictal confusion, headache, dysphasia, nose rubbing
o Second generation seizure less common
Occipital lobe - normal role
Vision
Occipital lobe seizures
Visual hallucinations
Visual disturbances – unformed, circular, multi-coloured, confined to hemifield
What is the most common type of seizure?
Focal that originates in temporal lobe and then spread to generalised
Tonic seizure
Increased tone of postural muscles
Function of pinna (auricle)
To funnel sound into ear canal and can pick up human speech over background noise
Myoclonic seizure
Involuntary movements that can involve the whole body or just parts of it
Secondary generalised seizures
- Temporal only
- Partial seizure where the epileptic discharge spreads to both cerebral hemispheres
- Once the discharge reaches the RAS, consciousness is lost - Results in generalised seizure
Anatomy of external auditory meatus
- Sigmoid canal
- 7mm diameter
- 25mm long
- 1st 1/3rd surrounded by cartilage
- 2/3rd surrounded by bone
- Cells in cartilaginous zone include: hair, sebaceous, ceruminous glands
Function of external auditory meatus
Amplifies sound
Syncope
- Sudden loss of consciousness with loss of postural muscle tone
- Due to reduced cerebral perfusion
Orthostatic hypotension
Syncope when standing up
Anatomy of tympanum
Collagenous membrane
