Causes of aortic stenosis
Senile calcification (60+)
Congenital: biscupid valve (40-60 years), Williams syndrome
Rheumatic fever
What is the commonest cause of aortic stenosis
Senile calcification
Features of Williams syndrome
Neurodevelopmental disorder characterised by “elfin” facies + low nasal bridge, cheerful demeanor and ease with strangers
Developmental delay
Language deficiencies
Profound visuo-spatial impairment
CV problems e.g. supravalvular aortic stenosis
Transient hypercalcaemia
Symptom triad in AS
Angina
Dyspnoea
Syncope (especially with exercise)
Symptoms of AS
Triad: angina, dyspnoea, syncope
LVF: PND, orthopnea, frothy sputum
Arrhythmias
Systemic emobli if endocarditis
Sudden death
Triad: angina, dyspnoea, syncope
LVF: PND, orthopnea, frothy sputum
Arrhythmias
Systemic emobli if endocarditis
Sudden death
Aortic stenosis
Def: supravalvular aortic stenosis
Congenital obstructive narrowing of the aorta above the aortic valve
Signs of AS
Slow rising pulse with narrow pulse pressure
Aortic thrill
Forceful, non-displaced apex (pressure overload)
Abnormal heart sounds:
Quiet A2
Early systolic ejection click if pliable (young valve)
S4: forceful atrial contraction vs hypertrophied valve.
Murmur:
ESM, right 2nd ICS sitting forward in end-expiration
Radiating to carotids
Abnormal heart sounds:
Quiet A2
Early systolic ejection click if pliable (young valve)
S4: forceful atrial contraction vs hypertrophied valve.
Aortic stenosis
Murmur:
ESM, right 2nd ICS sitting forward in end-expiration
Radiating to carotids
Aortic stenosis
What are the clinical indicators of severe AS?
Quiet/absent A2
S4
Narrow pulse pressure
Decompensation: LVF
DDx of AS
CAD
MR
Aortic sclerosis
HOCM
What differentiates clinically between AS and aortic scleorsis
Valve thickening rather than valve narrowing: no pressure gradient
Turbulence leads to mumrmur
ESM without radiation and a normal pulse
Doesn’t have the narrow PP, slow rising pulse, forceful apex or ECG evicednece of LVF seen in Aortic Stenossi
Ix in AS
FVC
U+E
Lipids
Glucose
What differentiates between HOCM and AS clinically
HOCM is an ESM murmur which increases intensity with the valsalva (reduces in AS)
ECG findings in AS
LVH
LV strain: tall R, ST depression, T inversion in V4-6
LBBB or complete AV block due to septal calcification (may need pacing)
CXR findings in AS
Calcified AV (esp on lateral films) LVH
Evidence of failure
Post-stenotic aortic dilatation
Aortic stenosis
Arrow= post stenotic dilatation
What is diagnostic in AS?
Echo+ doppler
Echo findings in AS
Thickened, calcified immobile valve cusps
Can be used to categorise severity
What Ix to perform in AS
Bloods
ECG
CXR
Echo+Doppler
Cardiac catheteristaion and angiography
Exercise stress test contraindicated if symptomatic)
Aortic stenosis
Echocardiography: severe AS
>4,/s jet velocity
>40mmHg pressure gradient
Valve area <1cm^2
Use of cardiac catheterisation and angiography in AS
Can assess valve gradient and LV function
Assess coronaries in all patients planned for surgery
Use of exercise stress test in AS
Contraindicated if symptomatic
May be useful to assess exercise capacity in asymptomatic patients
Medical Mx of AS
Optimise RFs: statins, anti-hypertensives, DM
Monitor with regular F/U (echo)
Angina: beta blockers
Heart failure: ACEI and diuretics
Avoid nitrates
Surgical mx of AS
Mechanical/biproshetic
Balloon valvuloplasty
TAVI
Implications of surgical replacement of valve in AS
Poor prognosis if symptomatic
Angina/syncope: 2-3y
LVF: 1-2y
Indications for valve replacement in AS
Severe symptomatic AS
Severe asymptomatic AS with reduced EF (<60%)
Severe AS undergoing CABG or other valve operation
Mechanical vs bioprosthetic valves
Mechanical last longer but need anticoagulation (used in younger patients)
Bioprosthetic: don’t require anticoagulation but fail sooner
Use of balloon valvuloplasty in AS
Limited use in adults as complication rate is high (>10%) and restenosis occurs in 6-12mo
Features of TAVI
Folded valve deployed in aortic root
Increased perioperative stroke risk cf. replacement
Reduction in major bleeding
Similar survival at 1y
Little long term data
Cx of TAVI
Major bleeding from entry sites
Stroke
VT
MI
Aortic dissection
Cardiac tamponade
Postoperative AR and paravalvular leak
CXR findings in pulmonary oedema
ABCDE
Alveolar shadowing
Kerley B lines
Cardiomegaly (cardiothoracic ratio >50%)
Diversion of the upper lobe
Effusions
Fluid in the fissures
Def: obstructive sleep apnoea
Intermitten closure/collapse of the pharyngeal airway-> apnoeic epsiodes duriing sleep
RFs for sleep apnoea
Obesity
Male
Smoker
EtOH
Idiopathic pulmonary fibrosis
Structural airway pathology e.,g. micrognathia
NM disease e.g. NMD
Ix in OSA
SpO2
Polysomnography is diagnostic
Rx of sleep apnoea
Weight loss
Avoid smoking and EtOH
CPAP during sleep
Surgery to relieve pharyngeal obstruction: tonsillectomy, uvulopalatpharyngoplasty
Clinical features of obstructive sleep apnoea
Nocturnal
Snoring
Choking, gasping, apnoeic episodes
Daytime:
Morning headache
Somnolence
Reduced memory and attention
Irritability, depression
Cx of obstructive sleep apnoea
Pulmonary HTN
T2 respiratory failure
Cor pulmonale
Assessment scores for sleep Apnoea
Epworth score ( fallling asleep in various situations)
STOP BANG
Autonomic complications of DM
Postural hypotension: Rx: fludorcortisone
Gastroparesis: early satiety, GORD, bloating
Diarrhoea: Rx: codeine phosphate
Urinary retention
Erectile dysfunction
RFs for aspiration pneumonia
Stroke
Bulbar palsy
Reduced GCS
GORD
Achalasia
Mx of aspiration pneumonia
Anaerobes
Co-amoxiclav PO TDS for 7D
What is risk feeding
Feeding in individual with unsafe swallow at risk of aspiration
e.g. not able to tolearte NG tube
Def: splinted diaphragm
Inhibition of diaphragmatic movement, seen in a variety of disease
Draw Einthoven’s triangle
Draw cardiac electrogram
Draw ECG lead arrangement
Draw cardiac conduction pathways
View: Leads II, III, aVf
Inferior
View: I, aVL, V5 + V6
Lateral
View: V2-V4
Anteroseptal
View: V2-V6
Anterolateral
View: V1, V2, V3 (reciprocal)
Posterior
Vessel: II, III, aVF
RCA
Vessel: I, aVL, V5 + V6
L circumflex
Vessel: V2-V4
LAD
Vessel: V2-V6
Left main stem
Rate on ECG
300/ no of large squares
If irregular, use rhythmn strip x 6
Componenets of reporting ECG
Demographics
Rate, rhythmn
Axis
P waves
QRS
PR interval
QTc
ST segments
T waves
Extras
https://www.youtube.com/watch?v=7lcm1HI4fbk
Def: MEN
Autosomal dominant functioning hormone tumours in multiple organs
MEN1
3 Ps
Parathyroid: adenoma/hyperplasia
Pituitary: adenoma, prolactin or GH
Pancreatic tumours: gastrinoma or insulinoma
MEN2A
2Ps 1 M
Thyroid medulary carcinoma
Parathyroid
Phaeochromocytoma
Hyperthyroidism
MEN2B
1P 2Ms
Phaeochromocytoma
Medullary thyroid carcinoma
Marfanoid habitus/,icosal neuroma
Def: DM
Multisystem disorder due to an absolute or relative lack of endogenous insulin leading to metabolic and vascular complications
Pathophysiology of T1DM
Auotimmune destruction of beta cells leading to an absolute insulin deficiency
Presentation of T1DM
Polyuria, polydipsia, weight loss, DKA, starting before puberty
Polyuria, polydipsia, weight loss, DKA, starting before puberty
T1DM
What HLAs associated with T1DM
HLA-D3 and D4
Anti-islet
Anti-GAD abs
T1DM
Pathophysiology of T2DM
Insulin resistance and beta cell dysfunction leading to relative insulin deficiency
Presentation of T2DM
Polyuria, polydipsia, complications
Concordance of T2DM
80% in MZs
Associations of T2DM
Obesity
Reduced exercise
Calorie and EtOH excess
Diagnostic criteria for DM, symptomatic
Symptoms i.e. polyuria, polydipsia, weight loss, lethargy
+
Raised plasma venous glucose detected once:
fasting >7mM
Random >11.1mM
Diagnostic criteria for DM, asymptomatic
Raised venous glucose detected on 2 separate occasions
or 2h OGTT >11.1
When is OGTT required?
When borderline fasting or random glucose measurements
Normal fasting glucose
<6.1
Normal OGTT
<7.8
Impaired fasting glucose
6.1-6.9
Impaired glucose tolerance
75g OGTT 7.8-11
Fasting glucose in DM
>7
75g OGTT in Diabetes
>11.1
Secondary causes of DM, drugs
Steroids
Anti-HIV
Atypical neuroleptics
Thiazides
Secondary causes of DM. pancreatic
CF
Chronic pancreatitis
Hereditary haemochromatosis
Pancreatic Ca
Secondary causes of DM, endocrine
Phaeo,
Cushings
Acromegaly
T4
Secondary causes of DM, other
GSDs
Def: Metabolic syndrome
Central obesity (raiesd waist circumference) and >1 of:
Raised TGs
Reduced HDL
HTN
Hyperglycaemia: DM, IGT, IFG
MDT mx of DM
GP
Endocrinologist
Sx
DSN
Dieticians
Chiropodists
Fellow patients
What are the 4Cs of DM monitoring
Control, glycaemiic
Complication
Competency
Coping
Monitoring DM: Control
Record of complications: DKA, HONK, hypos
Capillary blood glucose:
Fasting 4.5-6.5
2h post-prandial 4.5-9
HbA1c reflects exposure over last 6-8w
Aim 45-50 (7.5-8%)
BP, lipids
Monitoring Dm, Cxs
Macro: pulses, BP, cardiac auscultation
Micro: fundoscopy, ACR + U+Es, sensory testing plus foot inspection
Monitoring DM: Competency
With insulin injections
Checking injection sites
BM monitoring
Monitoring DM: coping
Psychoscoial e.g. ED, depression
Occupation
Domestic
Lifestlye modificaiton in DM: DELAYS
Diet
Exercise
Lipids
ABP
Asprin
Yearly/6 monthly check up: 4Cs
Smoking cessation
Lifestyle modificaiton, DM, diet
Same as that considered healthy for everyone
Reduced total calorie intake
Reduced refined carbs
Increased complex carbs
Increased soluble fibre
Reduced fat (sat)
Reduced Na
Avoid binge drinking
Lifestyle modification DM, lipis
Rx of hyperlipidaemia
Priamry prevention with statins if >40y regardless of lipids
Lifestyle modification DM, ABP
Reduce Na intake and EtOH
Keep BP <130/80
ACEI best, if afrocarribean descent ACEI + CCB or thiazide
Issue with beta blockers in DM?
Mask hypos
Issue with thiazides in DM
Raise glucose
Antiplatelet therapy in DM
Not recommended as primary prevention unles CVD
How can the VOR be used to determine whether a comatose patient’s brainstem is intact?
In comatose patients, once it has been determined that the cervical spine is intact, a test of the vestibulo-ocular reflex can be performed by turning the head to one side. If the brainstem is intact, the eyes will move conjugately away from the direction of turning (as if still looking at the examiner rather than fixed straight ahead). Negative “doll’s eyes” would stay fixed midorbit, and having negative “doll’s eyes” is therefore a sign that a comatose patient’s brainstem is functionally not intact.
Brown’s syndrome
Brown’s syndrome is a rare form of strabismus characterized by limited elevation of the affected eye. The disorder may be congenital (existing at or before birth), or acquired. Brown syndrome is caused by a malfunction of the Superior oblique muscle, causing the eye to have difficulty moving up, particularly during adduction (when eye turns towards the nose)
Draw the movements performed by the eye muscles
Characteristic of internuclear opathlmogpleiga
Paresis of eye adduciton in horizontal gaze but not in convergence
Due to lesions on the medial longitudinal fasciculus
Internuclear ophthalmoplegia results from a lesion in the MLF. In young people, the disorder is commonly caused by multiple sclerosis and may be bilateral. In the elderly, internuclear ophthalmoplegia is typically caused by stroke and is unilateral. Rarely, the cause is Arnold-Chiari malformation, neurosyphilis, Lyme disease, tumor, head trauma, nutritional disorders (eg, Wernicke encephalopathy, pernicious anemia), or drug intoxication (eg, with tricyclic antidepressants or opioids).
If a lesion in the MLF blocks signals from the horizontal gaze center to the 3rd cranial nerve, the eye on the affected side cannot adduct (or adducts weakly) past the midline. The affected eye adducts normally in convergence because convergence does not require signals from the horizontal gaze center. This finding distinguishes internuclear ophthalmoplegia from 3rd cranial nerve palsy, which impairs adduction in convergence (this palsy also differs because it causes limited vertical eye movement, ptosis, and pupillary abnormalities).
During horizontal gaze to the side opposite the affected eye, images are horizontally displaced, causing diplopia; end nystagmus often occurs in the abducting eye. Sometimes vertical bilateral nystagmus occurs during attempted upward gaze.
++ Urea
+Cr
+ Albumin
+ HCt
?Dehydration
+Urea
+Cr
+H
+K
+Urate
+PO4
Reduced Ca
?Low GFR
Low Na
Low K
Raised HCO3
Raised Urea
Thiazide and loop diuretics
Normal Urea and Creatinine
Reduced urate
Reduced PO4
Reduced HCO3
?Tubular dysfunction
Raised bilirubin
Raised ALP
Reduced albumin
Raised PT (Raised APTT if end stage)
Hepatocellular disease
Raised bilirubin
Raised ALP
Reduced albumin
Raised PT (Raised APTT if end stage)
AST:ALT >2, raised GGT
Alcoholic hepatocellular disease
Raised bilirubin
Raised ALP
Reduced albumin
Raised PT (Raised APTT if end stage)
AST:ALT <2
?Viral hepatocellular disease
Raised ALP
Raised GGT
Raised bilirubin
Raised AST
Cholestasis
Raised GGT
Raised MCV
Evidence of hepatocellular disease
?XS EtOH intake
Raised K
Reduced Na
?Addison’s
May show
Reduced K
Raised Na
Raised HCO3
?Cushing’s
Reduced K
Raised Na
Raised HCO3
?Conn’s
Raised Na
Raised serum osmolality
Reduced urine osmolality
DI
Reduced Na
Reduced serum osmolality
Raised urine osmolality
Raised urine Na
?SIADH
Presentation of hyponatraemia <135
N/v, anorexia, malaise
Presentation of hyponatraemia: <130
Headache, confusion, irritability
Presentation of hyponatraemia: <125
Seizures
Non-cardiogenic pulmonary oedema
Presentation of hyponatraemia <115
Coma and death
Causes of hypovolaemic hyponatraemia
U Na >20mM
= renal loss
Diuretics
Addison’s
Osmolar diuresis e.g. glucose
Renal failure (diuretic phase)
Causes of hypovolaemic hyponatreamia
U<20mM
=extra-renal loss
Diarrhoea
Vomiting
Fistula
SBO
Burns
Causes of hypervolaemic hyponatraemia
Cardiac failure
Nephrotic syndrome
Cirrhosis
Renal failure
Causes of euvolaemic hyponatraemia
U osmolality >500
SIADH
Causes of euvolaemic hyponatreamia
U osmolality <500
Water overload
Severe hypothyroidism
GC insufficiency
Mx of hyponatraemia
Correct the underlying cause
Replace Na and water at the same rate at which they were lost
NB: too fast-> central pontine myelinolysis
Rate of correction in chronic hyponatraemia?
10mM/d
Rate of correction in acute hyponatraemia?
1mM/hr
Mx of asymptomatic chronic hyponatraemia
Fluid restrict
Mx of symptomatic/acute hyponatraemia/dehydration
Cautious rehydration with 0.9% saline
Mx of hypervolaemic hyponatraemia
Consider frusemide
Mx of hyponatraemia if seizures/coma
Consider hypertonic saline
Def: SIADH
Concentrated urine: Na >20mM, osmolality >500
Hyponatraemia or palsma osmolality <275
Absence of hypovolaemia, oedema or diuretics
Causes of SIADH
Resp
CNS
Endo
Drugs
Resp: SCLC, pneumonia, TB
CNS; meningoencephalitis, head injury, SAH
Endo: hypothyroidism
Drugs: cyclophosphamdie, SSRIs, CBZ
Which drugs can cause SIADH
Cyclophosphamide, SSRIs, CBZ
Rx in SIADH?
Rx cause and fluid restrict
Consider vasopressin R antagonists: demclocycline, vaptans
Blood supply of the spinal cord
3 longitudinal vessels:
2 posterior spinal arteries- dorsal 1/3
1 anterior spinal artery: ventral 2/3
Reinforced by segmentel feeder arteries
Longitudinal veins drain intot he extradural vertebral plexus
Gross anatomy of the spinal cord
Foramen magnum to L1/L2
Terminates as conus medullaris
Spinal nerves continue inferiorly as cauda equina
Denticulate ligament and filum terminale are pial extensions that supend the cord in subarachnoid space
The spinal dura mater is continueous with what?
The neuronal epineurium
In what spinal mater is the CSF found?
The subarachnoid space
What level does the spinal cord finish at?
L1/L2
Describe the formation of spinal nerves
Mixed nerves that originate from the SC forming the peripheral nervous system
Each spinal nerve begins as an anterior (motor) and posterior (sensory) nerve root.
These arise from the spinal cord and unite at the intervertebral foramina forming a single spinal nerve
These nerves leave the vertebral canal and divide into two:
Anterior rami: nerve fibres to the body, both motor and sensory
Posterior rami: nerve fibres to the synovial joints of the vertebral column, deep muscles of the back and the overlying skin.
Muscle weakness, paralysis with loss of reflexes
Most commonly caused by vertebral fractures or dislocation, vasculitic disease, arethomatous disease or external compression
Spinal cord infarction
Where are 95% of spinal cord ischaemic events?
To the anterior aspect of the spinal cord, with the psoterior columns preserved
Modality of the dorsal columns?
Fine touch, vibration, proprioception
Cell body of the dorsal column?
DRG
Decussation of the dorsal column
In medulla, forming the medial leminicus
Mode of the lateral corticospinal tract
Motor (body)
Cell body of the spinothalamic tract
DRG
Decussation of the lateral spinothalamic tract
In cord, at entry level
Mode of the lateral corticospinal tract
Motor
Cell body of the lateral corticospinal tract
1o motor cotrex
Decussation of the lateral corticospinal tract
Pyramidal decussation in the ventral medulla
How can the somatosensory tracts be classified?
Conscious: dorsal column-medial leminiscal pathway and the anterolateral system
Unconscious: spinocerebellar
Organisation of the dorsal column-medial lemniscal pathway
3 groups
1o neurones: carry sensory information from receptors to the medulla. Signals from the upper limb travel in the fasciculus cuneatus (lateral part of the dorsal column) synapsing in the cuneate nucleus
Signals from the lower limb travel in the fasciculus gracilis (medial part) and synapse in the gracile nucleus)
2o:
Begin in either of the nuclei, synapse with 3o neurones in the thalamus. Decussate in the medulla oblongata and travel in the contralateral medial lemniscus to reach the thalamus.
3o:
Take sensory signals from the thalamus to the primary sensory cortex of the brain.
What is this pathway
DCML
Organisation of the anterolateral system
Two tracts:
Anterior spinothalamic: crude touch and pressure
Lateral spinothalamic: pain and temperature
1o:
Arise from sensory Rs in the periphery, enter the SC, ascend 1-2 levels and terminate at the tip of the dorsal horn (substantia gelatinosa)
2o:
Carry info from the susbtantita gelatinosa to the thalamus. Arise from synapse with 1o neurone, decussate and here the fibres split into the anterior and lateral tracts. Syanpse in the thalamus
3o
Take sensory signals from the thalamus to the primary sensory cortex of the brain, ascend from the ventral posterolateral nucleus of the thalamus, through the internal capsule, terminating at the sensory cortex
What info is carried by the anterior spinothalamic tract?
Crude touch and pressure
What info is carried by the lateral spinothalamic tract
Pain and temperature
What neural pathway is this?
Spinothalamic
What are the individual pathways in the spinocerebellar tracts?
Posterior spinocerebellar tract: proprioceptive info from lower limbs to the ipsilateral cerebellum
Cuneocerebellar tract: carries proprioceptive information from the upper limbs to the ipsilateral cerebellum
Anterior spinocerebellar tract: carries proprioceptive information from lower limbs, decussating twice and terminating in the ipsilateral cerebelllum
Rostral spinocerebellar tract: carries proprioceptive information from the upper limbs to the ipsilateral cerebellum
Pattern of sensory loss if DCML lesion in the spinal cord?
Ipsilateral dorsal modalities
Pattern of loss in injury to the anterolateral system
Contralteral pain and temperature sensation
Brown Sequard Syndrome pattern of loss
DCML: ipsilateral loss of tactile sensation and proprioception
Anterolateral system: contralateral loss of ppain and temperature sensation
Will also involve the descending motor tracts causing ipsilateral hemiparesis
Function of thalamic VPL nuceli
Somatosensory body
Function of thalamic VPM nuclei
Somatosensoty head
Function of thalamic LGN nuclei
Visual
Function of thalamic MGN nuclei
Auditory
How can the descending tracts be classified?
Pyramidal tracts: originate in the cerebral cotex, carry motor fibres to the spinal cord and brainstem: voluntary control
Extrapyramidal tracts: originate in the brainstem, carry motor fibres to the SC- responsbile for involuntary and automatic control of all musculature.
No synapses within the descending pathways.
How can the pyramidal tracts be classified?
Corticospinal: musculature of the body
Corticobulbar: musculature of the head and neck
Path of the corticospinal tracts
Begin in the cerebral cortex (primary motor cortex, premotor cortex, supplementary motor area)
Neurones converge and desced through the internal capsule
After the internal capsule the neurones pass through the crus cerebri of the midbrain, the pons and into the medulla.
In the most inferior part of the medulla the tract divides in two.
Fibres within the lateral corticospinal tract decussate and terminate in the ventral horn
Anterior spinal tract remains ipsilateral, they then decussate and terminate in the ventral horn of the cervical and upper thoracic segmental levels.
What is this pathway
Pyramidal: corticospinal pathway
Path of the corticobulbar tracts
Arise from the lateral aspect of the 1o motor cortex, receiving the same inputs as the corticopsinal tracts.
The fibres converge and pass through the internal capsule to the brainstem.
The neurones terminate on the motor nuclei of the cranial nerves. Here, they synapse with LMNs, which carry the motor signals to the face and neck.
NB many of these corticobulbar fibres innervate the motor neurones bilaterally. E.g. the fibres from the left 1o motor cortex act as UMNs
Upper motor neurones for the facial nerve have a contralateral innervation, this only affects muscles in the lower quadrant of the face, below the eyes
UMNs for hypoglossal only provide contralateral innervation
UMN innervation of the facial nerve
Upper motor neurones for the facial nerve have a contralateral innervation, this only affects muscles in the lower quadrant of the face, below the eyes
UMN innervation of the hypoglossal
Only provides contralateral innervation
What are the extrapyramidal tracts?
Vestibulospinal
Reticulospinal
Rubrospinal
Tectospinal
Which extrapyramidal tracts decussate?
Rubrospinal and tectospinal, therefore provide contralateral innervation
Function of the vestibulospinal
Two pathways: medial and lateral
Arise from vestibular nuclei which receive input from the organs of balance, they convey this info to the SC where it remains ipsilateral.
Fibres in this patheway control balance and posture via lower motor neurones
Functions of the reticulospinal tracts
Medial: arises from the pons, facilitates voluntary movements and increases muscle tone
Lateral: arises from the meudlla, inhibits voluntary movements and reduces muscle tone
Function of the rubrospinal tracts
Originates from red nucleus.
May play a role in fine control of hand movements
Function of the tectopsinal tracts
Begins at the superior colliculus of the midbrain. (receives input from optic nerves)
Neurones decussate
Tectospinal tract coordinates movements of the head in relation to visual stimuli)
Supranuclear lesions=
UMN
UMN lesion to the hypoglossal
A lesion to the upper motorn neurone will result in spastic paralysis of the contralateral side of genioglossus.
Tongue points to the contralateral side i.e. away from lesion
Function of cerebellum and BG
Output to cortex via thalamus
Regulation of posture, locomotion, coordination and movement
What is the internal capsule
White matter carrying axonal fibres from motor cortex to pyramids of medullla
Infarction can lead to contralateral hemiparesis
Function of the frontal lobe
Cognition and memory
Executive function
Motor cortex
Dominant hemisphere: motor speech (Broca’s area)
Function of the parietal lobe
Sensory cortex
Body orientation
Function of the temporal lobe
Memory
Dominant hemisphere: receptive language (Wernicke’s area)
Function of the occipital lobe
Visual cortex
Draw the homunculus
How can you differntiate between primary motor and primary somatosensory cortices
Primary somatosensory is posterior to the central sulcus
Draw the blood supply of the brain
Brainstem rule of 4
4 structures in the midline beginning with M
4 structures to the side beginning with S
4 cranial nerves in the medulla, 4 in the pons and 4 above the pons
4 motor nuclei that are in the midline are those that divide equally into twleve except for 1 and 2: 3, 4, 6, 12
(5,7,9,11 are in the lateral brainstem)
Brainstem rule of 4:
4 medial structures
1: motor pathway (corticospinal tract)
2: medial lemniscus: CL loss of viration and proprioception int he arm and leg
3: MLF: ipsilateral internuclear opthalmoplegia
4: motor nucleus and nerve (3, 4, 6, 12)
Brainstem, rule of 4
Lateral structures
Spinocerebellar pathway: ipsilateral ataxia of the arm and leg
Spinothalamic pathway: contralateral alteration of pain and temperature sensation affecting arm and leg
Sensory nucleus of Trigeminal: ipsilateral alteration of pain and T sensation in the trigeminal nerve distribution
Sympathetic pathway: ipsilateral horner’s: partial ptosis and a miosis
Brainstem rule of 4:
4 CNs in the medulla
9: loss of pharyngeal sensation
10; ipsilateral palatal weakness
11: spinal accessory: ipsilateral wekkness of the trapezius and sternocleidomastoid
12: hypoglossal: ipsilateral weakness of the tongue.
Brainstem rule of 4
4 cranial nerves in the pons
5: ipsilateral atleration of pain, T and light tocuh fo the face, sparing the angle of the jaw
6: ipsilateral weakness of eye abduction
7: ipsilateral facial wekaness
8: ipsilateral deafness.
Brainstem rule of 4
The 4 cranial nerves above the pons
Olfactory
Optic (not in midbrain)
Oculomotor:down and out, dilated pupil ipsilaterally
Trochlear: inability to look down when the eye is adducted.
Blood supply of the brainstem
Medial arteries i.e. basilar, vertebral, anterior spinal artery
Lateral arteries: posterior cerebral and superior cerebellar, anterior inferior cerebellar
Medial brainstem syndromes:
Due to para-median branch occlusion
Lateral brainstem syndromes
Due to occlusion of the circumferential branches also seen in unilateral vertebral occlusion.
If there are signs of both a lateral and medial brainstem syndrome?
?Basilar artery problem
Process of NMJ transmission
Presnyaptic volatge gated Ca channels open
ACh released from presynaptic terminal
ACh diffuses across cleft
ACh binds to nicotinic receptors on the post-synaptic terminal
Na influx, leads to depolarisation and SR Ca release, leading to muscle contraction
ACh degraded by acetylcholinesterase and choline is taken up into the presynaptic terminal
Targets for NMJ blockade
Block presynaptic chonline uptake: hemicholinium
Block ACh vesicle fusion: botulinum, LEMS
Block nAChR-
Non-depolarising: atracurium, vecuronium
Depolarsing: suxamethonium
What are the dopamine pathways in the brain?
Mesocorticolimbic: SCZ
Nigrostriatal: Parkinsonism
Tuberoinfundibular: Hyperprolactinaemia
Features of the sympathetic nervous system
Cell bodies from T1-L2
GVE preganglionic fibres synapse at either the paravertebral ganglia, the prevertebral ganglia or chromaffin cells of the adrenal medulla
Preganglionic fibres are myelinated and release ACh at nACHRs
Postganglionic fibres are unmyelinated and release NA at adrenergic receptors except at sweat glands where they release ACh for muscarinic Rs
What are the components of the parasympathetic nervous system?
Cranial: CN3, 7, 9, 10
Ciliary, pterygopalatine, submandibular, otic ganglions
Vagus supplies thoracic and abdominal viscera
Sacral: pelvic splanchnic nerves (S2-4) innervate the pelvic viscera
Preganglionic fibres release ACh at nAChRs, post-ganglionic fibres relase ACh at mAChRs
Funciton of ciliary ganglion
Ciliary muscle and sphincter pupillae
Function of pterygopalatine ganglia
Mucous membranes of the nose, palate and lacrimal gland
Function of the submandibular ganglion
Submandibular and sublingual glands
Functions of the otic ganglion
Parotid gland
Midbrain CN nuclei
3, 4 (5)
Pons CN nuclei
5,6,7,8
Medullla CN nuclei
5,8,10,11,12
VOR
Axons from vestibular neuornes project via MLF to abducens and oculomotor nuclei
Head turns L eyes trun R
Absent Doll’s eye sign= brainstem death
Features of caloric test of vestibulocoular pathway
Warm-> increased firing of vestibular neurones-> eye turns to the contralateral side with nystagmus to ipsilateral side
Remember fast direction of nystagmus:COWS
Cold: opposite
Warm: Same
Absence of eye movements= brainstem damage on side being tested
Which nucleus is involved in the pupillary light reflex?
Direct: Optic nerve-> Edinger Westphal nucleus-> ipsilateral pretectal nucleus, Oculomotor nerve synpases in ciliary ganglion leading to constriction of sphincter pupillae
Consensular: Optic nerve-> Edinger Westphail-> contralateral pretectal nucleus-> oculomotor nerve-> ciliary ganglion-> sphincter pupillae
Pattern of cortical motor deficit?
Hypereflexia proximally in arm or leg
Unexpected patterns e.g. all movements in hand/foot
Hypereflexia proximally in arm or leg
Unexpected patterns e.g. all movements in hand/foot
?Cortical lesion
Pattern of lesion to internal capsule and corticospinal tracts?
Contralateral hemiparesis with pyramidal distribution
Lesion with epilepsy, reduced cognition or homonymous hemianopia= in cerebral hemisphere
Lesion with contralateral CN palsy= brainstem lesion on the side of the palsy (e.g. Miilar-Gubler syndrome)
Contralateral hemiparesis with pyramidal distribution
?Internal capsule/corticospinal lesion
Contralateral hemiparesis with pyramidal distribution
With epilepsy, reduced cognition or homonymous hemianopia
=In cerebral hemisphere
Contralateral hemiparesis with pyramidal distribution
With contralateral CN palsy=
Brainstem lesion on the side of the lesion
Milard-Gubler Syndrome
Lesion of the pons aka ventral pontine syndrome
Symptoms result from the functional loss of anatomical structures of the pons including CNVI and VII and fibres of the corticospinal tract
Paralysis of CNVI leads to diplopia, esotropia (internal strabismus) and loss of eye abduction
Disruption of CNVII leads to flaccid paralysis of the muscles of facial expression and loss of the corneal reflex
Disruption of the corticospinal tract leads to contralateral hemiplegia of the extermities
Lesion of the pons aka ventral pontine syndrome
Symptoms result from the funcitonal loss of anatomical structures of the pons including CNVI and VII and fibres of the corticospinal tract
Paralysis of CNVI leads to diplopia, esotropia (internal strabismus) and loss of eye abduction
Disruption of CNVII leads to flaccid paralysis of the muscles of facial expression and loss of the corneal reflex
Disruption of the corticospinal tract leads to contralateral hemiplegia of the extermities
Millar-Gubler syndrome
Patern of cord lesion with motor deficit
Quadriparesis/paraparesis
Motor and reflex level: LMN signs at level of the lesion and UMN signs below
Quadriparesis/paraparesis
Motor and reflex level: LMN signs at level of the lesion and UMN signs below
?cord lesion
Pattern of deficit in peripheral motor neuropathy
Usually distal weakenss
In GBS the weakness is proximal (root involvement)
Single nerve= mononeuropathy- trauma or entrapment
Several nerves= mononeuritis multiplex: vasculitis or DM
Causes of mononeuritis multiplex
Vasculitis or DM
Features of UMN lesions
Motor cells in pre-central gyrus to anterior horn cells in the cord
Pyramidal weakness: extensors in UL, flexors in LL
No wasting
Spasticity: increased tone +/- clonus
Hyperreflexia
Up-going plantars
Pyramidal weakness: extensors in UL, flexors in LL
No wasting
Spasticity: increased tone +/- clonus
Hyperreflexia
Up-going plantars
UMN lesion
Pattern of deficit in LMN lesions
Anterior horn cells to peripheral nerves
Wasting
fasciculation
Flaccidity: hypotonia
Hyporeflexia
Downgoing plantars
Anterior horn cells to peripheral nerves
Wasting
fasciculation
Flaccidity: hypotonia
Hyporeflexia
Downgoing plantars
LMN lesion
Pattern of deficit in primary muscle lesions
Symmetrical loss
Reflexes lost later than in neuropathies
No sensory loss
Fatiguability in myasthenia
Symmetrical loss
Reflexes lost later than in neuropathies
No sensory loss
Fatiguability in myasthenia
Primary muscle lesions
Patterns of sensory deficits
Pain and temp travel in small fibres in peripheral nerves and in anterolateral spinothalamic tracts
Touch, joint position and vibration travel in large fibres peripherally and in dorsal columns centrally
Distal sensory loss
Suggestive of a neuropathy
Sensory level tells us
Hallmark of cord lesion
Spinal nerves:
Neck flexor
C1-C6
Spinal nerves:
Neck extensors
C1-T1
Spinal nerves:
Supply diaphragm
C3, 4, 5
Spinal nerves:
C5, C6
Move shoulder, raise arm, flex elbow
Spinal nerves:
C6
Externally rotate (supinate the arm)
Spinal nerves:
C6-7
Extend elbow and wrist (triceps and wrist extensors)
Pronate wrist
Spinal nerves:
C7, T1
Flex wrist, supply small muscles of the hand
Spinal nerves:
T1-T6
Intercostals and trunk above the waist
Spinal nerves:
T7-L1
Abdominal muscles
Spinal nerves:
L1-L4
Flex thigh
Spinal nerves:
L2, L3, L4
Adduct thigh, extend leg at the knee (quadriceps femoris)
Spinal nerves:
L4, L5, LS1
Abduct thigh
Flex leg at the knee
Dorsiflex foot
Extend toes
Spinal nerves:
L5, S1, S2
Extend leg at the hip
Plantar flex foot
Flex toes
Ipsilateral loss of proprioception/vibration and UMN weakness with contralateral loss of pain
Brown-Sequard syndrome
Selective loss of pain and temp with conservation of proprioception and vibration (dissociated sensory loss)
Occurs in cervical cord lesions e.g. syringomyelia
Cerebellar syndrome
DDANISH
Dysdiadochokinesia
Dysmetria: past-pointing
Ataxia: limb/truncal
Nystagmus: horizontal= ipsilateral hemisphere
Intention tremor
Speech: slurred, staccato, scanning dysarthria
Scanning dysarthria
Scanning speech, also known as explosive speech, is a type of ataxic dysarthria in which spoken words are broken up into separate syllables, often separated by a noticeable pause, and spoken with varying force.
Causes of cerebellar syndrome
PASTRIES
Paraneoplastic: e.g. from bronchial carcinoma
Alcohol: thiamine and B12 deficiency
Sclerosis
Tumour e.g. CPA lesion
Rare: MSA, Friedrich’s, Ataxia Telangiectasia
Iatrogenic: phenytoin
Endo: hypothyroidsim
Stroke: vertebrobasilar
What does the ACA supply
Frontal and medial part of cerebrum
Contralateral motor/sensory loss in the legs>arms
Face spared
Abulia (pathological laziness)
ACA insult
What does the MCA supply
Lateral/external part of hemisphere
Contralateral motor/sensory loss in face and arms/legs
Contralateral homonymous hemianopia due to involvement of optic radiation
Dominant hemisphere (L): aphasia
Non-dominant hemisphere: neglect, apraxia
MCA insult
What does the PCA supply?
Occipital lobe
Contralateral homonymous heminaopia with macula sparing
PCA insult
What is supplied by the vertebrobasilar circulation?
Cerebellum, brainstem and occipital lobes
Any insult to this circulation can present with a combination of symptoms
Combination of symptoms from:
visual- hemianopia, cortical blindness
DANISH
CN lesions
Hemi/quadriplegia
Uni/bilateral sensory sympyoms
?Vertebrobasilar insult
Lateral Medullary syndrome as a consequence?
Occlusion of one vertebral A or PICA
Features of Lateral Medullary Syndrome (Wallenberg’s syndrome0
DANVAH
Dysphagia
Ataxia (ipsilateral)
Nystagmus (ipsilateral)
Vertigo
Anaesthesia: ipsilateral facial numbness and absent corneal reflex, contralateral pain loss
Horner’s syndrome
Millard-Gubler Syndrome (crossed hemiplegia)
Pontine lesion (e.g. infarct)
6th and 7th CN palsy with contralateral hemiplegia
Causes of locked in syndrome
Ventral pons infarction: basilar artery
Central pontine myelinolysis
Causes of CPA syndrome
Acoustic neuroma, meningioma, cerebellar astrocytoma, metastasis
Features of CPA syndrome
Ipsilateral CN5, 6, 7, 8 palsies and cerebellar signs
Absent corneal reflex
LMN facial palsy
LR palsy
Sensorineural deafness, vertigo, tinnitus
DANISH
Ipsilateral CN5, 6, 7, 8 palsies and cerebellar signs
Absent corneal reflex
LMN facial palsy
LR palsy
Sensorineural deafness, vertigo, tinnitus
DANISH
CPA Syndrome
What is subclavian steal syndrome
Subclavian artery stenosis proximal to the origin of the vertebral artery may lead to blood being stolen from this vertebral artery by retrograde flow
Syncope/presyncope or focal neurology on using the arm
Subclavian Steal Syndrome
Def: Subclavian Steal Syndrome
Syncope/presyncope or focal neurology on using the arm
BP difference >20mmHg between arms
Def: Beck’s Syndrome
aka Anterior Spinal Artery Syndrome
Infarction of spinal cord in distibution of anterior spinal artery (i.e. ventral 2/3rds of cord)
Causes of Anterior Spinal Artery (Beck’s syndrome)
Aortic aneurysm dissection or repair
Para/quadriparesis
Impaired pain and temperature sensation
Preserved touch and proprioception
Anterior Spinal Artery Syndrome
Structure of muscle weakness differential
Cerebrum/brainstem
Cord
Anterior horn
Roots/plexus
Motor nerves
NMJ
Muscle
Cerebral/brainstem causes of muscle weakness
Vascular: infarct, haemorrhage
Inflammation: MS
SOL
Infection: encephalitis, abscess
Cord causes of muscle weakness
Vascular: anterior spinal artery infarction
Inflammation: MS
Injury
Anterior horn causes of muscle weakness
MND, polio
Roots/plexal cause of muscle weakness
Spondylosis
Cauda equina syndrome
Carcinoma
Motor nerve causes of muscle weakness
Motorneuropathy e.g. compression
Polyneuropathy e.g. GBS, CMT
NMJ causes of muscle weakness
MG
LEMS (Lambert-Eaton)
Botulism
With what is myasthenia gravis assocaited?
Thymoma
Muscular causes of muscle weakness
Toxins: steroids
Poly/Dermato-myositis
Inherited: DMD, BMD, FSH
How can gait disturbance be classified?
Motor
Basal ganglia
UMN bilateral/unilateral
LMN unilateral/bilateral
Mixed UMN and LMN
Sensory
Vestibular
Cerebellar
Proprioceptive loss
Visual loss
Other
Basal ganglia causes of gait disturbance
Festinating/shuffling
PD
Parkinsonism: MSA, PSP, LBD, CBD
UMN bilateral cause of gait disturbance
Spastic, scissoring
Cord: compression, trauma, hereditary spastic paraparesis, syringomelia, transverse myelitis
Bihemispheric: CP, MS
Description of spastic gait
Scissoring- bilateral
Cricumducting- unilateral
LMN bilateral causes of gait disturbance
Bilateral foot drop
Polyneuropathy: CMT, GBS
Cauda equina
High stepping gait aka
Foot drop
Unilateral or bilateral
LMN uniltaeral causes of gait distrubance
Foot drop-> high stepping gait
Anterior horn: Polio
Radicular: L5 root lesion
Sciatic/common peroneal nerve: trauma. DM
Causes of mixed UMN and LMN gait disturbance
MND
Ataxia: Friedrich’s
SACD
Taboparesis
How can hand wasting differential be structured?
Cord
Roots
Plexus
Neuropathy
Muscle
Cord causes of hand wasting
Anterior horn: MND, polio
Syringomyelia
Root causes of hand wasting
Spondylosis, neurofibroma
Plexal causes of hand wasting
Compression: cervical rib, tumour: Pancoast’s, breast
Avulsion: Klumpke’s palsy
Neuropathic causes of hand wasting
Generalised: CMT
Mononeuritis multiplex: DM
Compressive mononeuropathy:
Median- thenar wasting
Ulnar- hypothenar and interossei wasting
Muscular causes of hand wasting
Disuse: RA
Compartment syndrome: Volkman’s ischaemic contracture
Distal myopathy: myotonic dystrophy
Cachexia
Volkman’s iscahemic contractiure
Permanent flexion contracture of the hand at the wrist
Causes of Volkmann’s ischaemic contracture
: esp those associated with vascular injury
Neglected compartment syndrome
Crush syndrome
Bleeding disorders
Iscahemic leading to contracture of long flexors and extensors in the forearm
Vestibular causes of gait disturbance
Romberg’s +ve:
Meniere’s
Viral labyrinthitis
Brainstem lesion
Cerebellar causes of gait disturbance
Ataxis
EtOH
Infarct
Proprioceptive causes of gait disturbance
Romberg’s +ve
Dorsal columns: B12 deficiency
Peripheral neuropathy: DM, EtOH, uraemia
Other causes of gait disturbance
Myopathy, MG/LEMS
Medical: postural hypotension, Stokes-Adams, arthritis
Causes of blackouts
CRASH
Cardiac
Arterial
Systemic
Head
Cardiac causes of blackouts
Stokes-Adams Attacks
Brady: heart block, sick sinus, long-QT
Tachy: SVT, VT
Structural: weak heat: LVF, tamponade.
Block: AS, HOCM, PE
What are the reflexes leading to blackout
Vagal overactvitiy
Sympathetic underactivity= Postural hypotension
Features of vagal overactivity
Vasovagal syncope
Situational: cough, effort, micturition
Carotid sinus syncope
Causes of postural hypotension
STANDUP
Salt deficiency: hypovolaemia, Addison’s
Toxins:
Cardiac- ACEI, diuretics, Nitratates, alpha blockers
Neuro: TCAs, benzos, antipsychotics, L-DOPA
Autonomic Neuropathy: DM, Parkinson’s GBS
Dialysis
Unwell: chronic bed rest
Pooling, venous: varicose veins, prolonged standing
Arterial causes of blackouts
Vertebrobasilar insufficiency: migraine, TIA (doesn’t really cause blackouts), CVA, subclavian steal
Shock
HTN: phaeo
Systemic causes of blackouts
Metabolic: reduced glucose
Respiratory: hypoxia, hypercapnia
Blood: anaemia, hyperviscosity
Head causes of blackout
Epilepsy
Drop attacks
Examination following black out
Postural hypotension: difference of >20/10 after standing for 3 mins vs lying down
CV
Neurological
Ix following blackout
ECG +/- 24hr ECG
U+E, FBC, Glucose
Tilt table
EEG, sleep EEG
Echo
CT
MRI brain
Triggers in cardiogenic syncope
Exertion, drug, unkown
Symptoms before in cardiogenic syncope
Palpitations, chest pain, dyspnoea
Symptoms during cardiogenic syncope
Pale, slow/absent pulse, clonic jerks may occur
Symptoms after cardiogenic syncope
Rapid recovery
ix in cardiogenic syncope
ECG
24hr ECG
Echo
Trigger for vasovagal syncop
Prolonged standing, heat, fatigue, stress
Symptoms before vasovagal syncope
Gradual onset: secs-> mins
Nausea, pallor, sweating, tunnel vision, tinnitus
Cannot occur lying down
Symptoms during vasovagal syncope
Pale, grey, clammy, bradycardic
Clonic jerks and incontinence can occur but no tongue biting
Symptoms after vasovagal syncope
Rapid recovery
Ix in vasovagal syncope
Tilt-table testing
Trigger to postural hypotensive blackout
Standing uo
Before during and after as for vasovagal
Ix in postural hypotension
Tilt-table testing
Trigger in arterial causes of blackout
Arm elevation, migraine
Before during and after in arterial blackouts
As for vasovagal +/- brainstem symptoms e.g. diplopia, nausea, dysarthria
Ix in arterial blackouts
MRA, duplex vertebrobasilar circulation
Symptoms of hypoglycaemia
Tremor, hunger, sweating, light-headedness-> LOC
Triggers in epilepsy
Flashing lights, fatigue, fasting
Symptoms before epileptic epsidoe
Aura in complex partial seizures- feeling strange epigastric rising
Deja/jamais vu
Smells
Lights
Automatisms
Symptoms during epileptic episode
Tongue biting
Incontinence
Stiffness-> jerking, eyes open
Cyanosis
Reduced SpO2
Symptoms after epileptic episode
Headache
Confusion
Sleeps
Todd’s palsy
Todd’s palsy
Post-ictal paresis/palsy
Usually confined to one side
Usually abates after 48hrs
Symptoms of drop-attack
Sudden weakness of legs causes older woman to fall to the ground
Features of drop attacks
No LOC
Sudden weakness
No post-ictal phase
Def: vertigo
The illusion of movement, usually rotatory of patient or surroundings
Worse on movement
Def: dizziness
With impaired consciousness= blackout
Without impaired consciousness
Vertigo: vestibular
Imbalance: vestibular, cerebellar, extrapyramidal
Causes of vertigo
IMBALANCE
Infection/injury
Meniere’s
BPV
Aminoglycosides/frusemide
Lymph
Arterial
Nerve
Central lesions
Epilepsy
Infective causes of vertigo
Labyrinthitis: post-viral severe vertiog, N+V
Ramsay Hunt
Trauma: to petrous temporal bone
Symptoms of Menniere’s
Recurrent vertigo (~20 mins) +/- N+V
Fluctuating SNHL
Tinnitus
Aural fullness
Lymph, peri, fistula causing imbalance
Connection between inner and middle ears
Traumatic or congenital
Presents with vertigo, SNHL
On examination Tullio’s phenomenon may be seen
Connection between inner and middle ears
Traumatic or congenital
Presents with vertigo, SNHL
On examination Tullio’s phenomenon may be seen
Lymph, Peri fistula
Connection between inner and middle ear
Tullio phenomenon
Tullio phenomenon, sound-induced vertigo, dizziness, nausea or eye movement (nystagmus) was first described in 1929 by the Italian biologist Prof. Pietro Tullio. (1881–1941)[1][2] During his experiments on pigeons, Tullio discovered that by drilling tiny holes in the semicircular canals of his subjects, he could subsequently cause them balance problems when exposed to sound.
The cause is usually a fistula in the middle or inner ear, allowing abnormal sound-synchronized pressure changes in the balance organs.[3] Such an opening may be caused by a barotrauma (e.g. incurred when diving or flying), or may be a side effect of fenestration surgery, syphilis or Lyme disease. Patients with this disorder may also experience vertigo, imbalance and eye movement set off by changes in pressure, e.g. when nose-blowing, swallowing or when lifting heavy objects.
Arterial causes of vertigo
Migraine
TIA/Stroke
Nerve causes of imbalance
Acoustic neuroma/vestibular schwannoma
Central lesions causing vertigo
Demyelination, tumour, infarct (e.g. LMS)
Epileptic causes of vertigo
Complex partial seizures
Conductive causes of hearing loss
WIDENING
Wax or foreign body
Infection: otitis media, OME
Drum perf
Extra: ossicle discontinuity- otosclerosis, trauma
Neoplasia: carcinoma
INury: barotrauma
Granulomatous: Wegener’s, Sarcoid
Sensorineural causes of hearing loss
DDIVINITY
Developmental
Degenerative
Infection
Vascular
Inflammation
Neoplasia
Injury
Toxins
lYmph
Developmental causes of sensorineural hearing loss
Genetic: Alport’s, Waardenburgs
Congenital: TORCH
Perinatal: anoxia
Degenerative causes of sensorineural hearing loss?
Presbyacusis
Infective causes of sensorineural hearing loss
VZV, measles, mumps, IFV
Meningitis
Vascular causes of sensorineural hearing loss
Ischaemia of internal auditory artery-> sudden hearing loss and vertigo
Stroke
Inflammatory causes of hearing loss
Vasculitis
Sarcoidosis
Neoplastic cause of sensorineural hearing loss
CPA tumours: acoustic neuroma
What is the commonest cause of unilateral SNHL
Acoustic neuroma
Toxins causing sensorineural hearing loss
Gentamicin
Frusemide
Aspirin
lYmph causes of sensorineural hearing loss
Endolymphatic hydrops= Menier’es
Perilymphatic fistula= ruptured round window
Def: tremor
Regular, rhythmic oscillation
Types of tremor
RAPID
Resting
Action/postural
Intention
Dystonic
Features of resting tremor
4-6Hz, pill-rolling
Abolished on voluntary movement
Increased with distraction (e.g. counting backwards)
Caused by Parkinsonism
Rx with Da agonists, antimuscarinic e.g. procyclidine
4-6Hz, pill-rolling
Abolished on voluntary movement
Increased with distraction (e.g. counting backwards)
Caused by Parkinsonism
Rx with Da agonists, antimuscarinic e.g. procyclidine
Resting tremor
Features of action/postural tremor
6-12Hz
Absent at rest
Worse with outstretched hands or movement
Equally bad at all stages of movement
6-12Hz
Absent at rest
Worse with outstretched hands or movement
Equally bad at all stages of movement
Action/postural tremor
Causes of postural tremor
BEATS
Benign essential tremor
Endocrine: thyrotoxicosis, reduced glucose, phaeochromocytoma
Alcohol withdrawal (or caffeine, opioids)
Toxins: beta agonists, theophylline, VPA, phenytoin
Sympathetic: physiological tremor may be enhanced e.g. anxiety
Features of intention tremor
>6Hz, irregular, large amplitude
Worse at end of movement e.g. past pointing
>6Hz, irregular, large amplitude
Worse at end of movement e.g. past pointing
Intention tremor
Cause of intention tremor
Cerebellar damage
Features of dystonic tremor
Variable
Causes are mostly idiopathic/ as for dystonia
Features of benign essential tremor
Autosomal dominant
Occur with action and worse with anxiety, emotion, caffeine
Arms, neck, voice
Doesn’t occur during sleep
Better with EtOH
Autosomal dominant
Occur with action and worse with anxiety, emotion, caffeine
Arms, neck, voice
Doesn’t occur during sleep
Better with EtOH
Benign essential tremor
Def: myoclonus
Sudden, involuntary jerk
Causes of myoclonus
Metabolic: asterixis (L, R, raised CO2)
Neurodegenerative diseases (lysosomal storage disorders)
CJD
Myoclonic epilepsies e.g. infantile spasms
Metabolic causes of asterixis
Hepatic flap (ammonia)
Renal flap (azotemia- urea)
Electrolyte: hypoglycaemia, hypokalaemia and hypomagnesaemia
Drugs: barbiturate, EtOH, phenytoin, primidone
Benign Essential Myoclonus
Autosomal dominant
Childhood onset, frequent generalised myoclonus without progression
May respond to valproate
Def: dystonia
Prolonged muscle contracture- unusual joint posture or repetitive movmenets
Idiopathic generalised dystonia
Often autosomal dominant
Childhood onset: starts in one leg and spreads on that side of the body over 5-10 years
Idiopathic focal dystonia
Commonest form of dystonia
Confined to one part of the body
Worsened by stress
What are the types of idiopathic focal dystonia?
Spasmodic torticollis
Blepharospasm
Oromandibular
Writer’s/Musician’s cramp
Types of acute dystonia
Torticollis, trismus and or occulogyric crisis
Trismus
Reduced opening of the jaw caused by spasm
Drugs causing acute dystonia
Neurlopetics
Metoclopramide (NB pregnant women)
L-Dopa
Rx in acute dystonia
Procyclidine (antimuscarinic)
Def: chorea
Non-rhythmic, purposeless, jerky, flitting movements
e.g. facial grimacing, flexing/extending the fingers
Causes of chorea
Huntington’s
Sydenham’s
Wilson’s
L-Dopa
Def: athetosis
Slow, sinuous, writhing movements
Causes of athetosis
Cerebal palsy
Kernicterus
Hemiballismus
Large amplitude, flinging hemichorea
Contralateral to a vascular lesion in the subthalamic nucleus: often in elderly diabetics
Recovers spontaneously over moths
Which region of the brain is involved in hemiballismus
Subthalamic nucleus
What causes tardive syndromes
Delayed onset following chronic exposure to dopamine antagonsts e.g. antipsychotics, antiemetics, L-Dopa
How can tardive syndromes be classified?
Dyskinesia: orobuccolingual, truncal or choreform movements
Dystonia: sustained, stereotyped muscle spasms of twitching or turning
Akathisia: unpleasant sense of inner restlessness +/- repetitive movements e.g. pacing
Rx in tardive syndromes
Change e.g. to atypical or slowly withdraw drug
Dyskinesia: tetrabenazine
Akathisia: beta blocker
Def: dementia
Chronically impaired condition that affects multiple domains without impairment of consciousness
Acquired and progressive
PC in AD
Progressive, global, cognitive decline
RFs for AD
ApoE4
Presenilin 1/2 muts
DS
Ix in AD
MRI- medial temporal lobe atrophy
Rx in AD
Cholinestarse inhibitors e.g. donepezil, rivastigmine if MMSE is 10-20
Ix in Vascular dementia
MRI- extensive infarcts or small vessel disease
Sudden onset, stepwise deterioration, patchy deficits in cognition
Vascular RFs
?Vascular dementia
Pathophysiology of LBD
Lewy Bodies in occipito-parietal cortex
Rx in vascular dementia
Manage predisposing factors
Fluctuating cogntiive dysfunction, visual hallucinations, parkinsonism
LBD
Rx in LBD
Cholinesterase inhibitors
Disinhibition, personality change, early memory preservation, progressive aphasia
Frontotemporal dementia
This is the most severe form of aphasia, and is applied to patients who can produce few recognizable words and understand little or no spoken language. may often be seen immediately after the patient has suffered a stroke and it may rapidly improve if the damage has not been too extensive. However, with greater brain damage, severe and lasting disability may result.
Global aphasia
In this form of aphasia, speech output is severely reduced and is limited mainly to short utterances of less than four words. Vocabulary access is limited and the formation of sounds is often laborious and clumsy. The person may understand speech relatively well and be able to read, but be limited in writingoften referred to as a ‘non fluent aphasia’ because of the halting and effortful quality of speech.
Broca’s aphasia
Expressive aphasia
This term is applied to patients who have sparse and effortful speech, resembling severe Broca’s aphasia. However, unlike persons with Broca’s aphasia, they remain limited in their comprehension of speech and do not read or write beyond an elementary level.
Mixed non-fluent aphasia
In this form of aphasia the ability to grasp the meaning of spoken words is chiefly impaired, while the ease of producing connected speech is not much affected. THowever, speech is far from normal. Sentences do not hang together and irrelevant words intrude-sometimes to the point of jargon, in severe cases. Reading and writing are often severely impaired.
Receptive aphasia (Wernicke’s)
This term is applied to persons who are left with a persistent inability to supply the words for the very things they want to talk about-particularly the significant nouns and verbs. As a result their speech, while fluent in grammatical form and output is full of vague circumlocutions and expressions of frustration. They understand speech well, and in most cases, read adequately. Difficulty finding words is as evident in writing as in speech.
Anomic aphasia
. Unlike other forms of aphasia that result from stroke or brain injury, PPA is caused by neurodegenerative diseases, such as Alzheimer’s Disease or Frontotemporal Lobar Degeneration. PPA results from deterioration of brain tissue important for speech and language. Although the first symptoms are problems with speech and language, other problems associated with the underlying disease, such as memory loss, often occur later.
Primary progressive aphasia
Ameliorable causes of dementia
Infection:
Viral: HIV, HSV, PML
Helminth: cysticerosis, toxo
Vascular:
Chronic SDH
Inflammation
SLE, carcoid
Neoplasia
Nutritional:
Thiamine deficiency
B12 and folate deficiency
Pellagra (B3/niacin deficiency)
Hypothyroid
Hypoadrenalism
Hypercalcaemia
Normal pressure hydrocephalus
(Depression)
Def: delerium
Globally impaired cognition and impaired consciousness
Disorientation to person, time and place
Reversal of sleep-wake cycle (hyperactive at night)
Labile mood
Illusions, delusions and hallucinations
Cognitive impairment: memory, language, concentration
Delirium
Causes of ACS
DELIRIUMS
Drugs: opiods, sedatives, L-DOPA
Eyes, ears and other sensory deficits
Low O2 states: MI, stroke, PE
infection
Retention
Ictal
Under-hydration/nutrition
Metabolic: DM, post-op, sodium ,uraemia
SDH or other intracranial pathology
Ix in ACS
Bloods: FBC, U+Es, LFTs, glucose, ABG
urine dip
Septic screen
ECG, LP
Mx of delirium
ID and Rx underlying cause
Surround with familiar people
Nurse in moderately, lit quiet room
Help to orientate to time and space
Find glasses, hearing aids
Avoid sedatives if possible but if disruptive@
Haldol 0.5-2mg PO/IM
Chlorpromazine 50-100mg PO/IM (avoid in elderly)
Causes of acute headache
VICIOUS
Vascular
Infection/inflammation
Compression
ICP
Opthalmic
Unknown
Systemic
Vascular causes of acute headache
Haemorrhage: SAH, intracranial, intracerebral
Infarction: esp. posterior circulation
Venous: sinus/cortical thrombosis
Infective/inflammatory causes of acute headache
Meningitis
Encephalitis
Abscesss
Compressive causes of acute headache
Obstructive hydrocephalus: tumour
Pituitary enlargement: apoplexy
bleeding into or impaired blood supply of the pituitary gland at the base of the brain. This usually occurs in the presence of a tumor of the pituitary, although in 80% of cases this has not been diagnosed previously. The most common initial symptom is a sudden headache, often associated with a rapidly worsening visual field defect or double vision caused by compression of nerves surrounding the gland. This is followed in many cases by acute symptoms caused by lack of secretion of essential hormones, predominantly adrenal insufficiency
Pituitary apoplexy
Reduced ICP causes of acute headache
Spontaneous intracranial hypotension: acute dural CSF leak
Worse on standing initially
Ophthalmic cause of acute headache
Acute glaucoma
Unknown causes of acute headache
Cough, exertion, coitus
Systemic causes of acute headache
HTN: Phaeo, pre-eclampsia
Infection: sinusitis, tonsillitis, atypical pneumonia
Toxins: CO
Causes of chronic headache
MCD TINGS
Migraine
Cluster headaches
Drugs:
Analgesics, caffeine, vasodilators: Ca2+ antatgonists, nitrates
ICP:
raised: tumour, aneurysm, AVM, benign intracranial HTN
reduced: spontaneous intracranial hypotension
Neuralgia
GCA
Systemic:
HTN
Organ failure: uraemia
Ix in headache
Blooods
Urine
Micro: cultures, serology (enterovirus), HSV, HIV, syphillis, crypto, CSF
Radiology:
Non-contrast CT
SAH: blood in sulci, cisterns, white: 90% sensitivity in first 24h
MRI: MRA: anerusym
MRV: sinus thrombosis
Special: CSF
What is the normal opening pressure of CSF?
5-20cm H2O
Raised opening pressure CSF
SAH, meningitis
Reduced CSF opening pressure
Spontaneous intracranial hypotension
Cause of CSF xanthochromia
Yellow appearnce of CSF due to bilirubin, detected by spectrophotometry
Blood in CSF e.g. in SAH
CSF:
Turbid apperance
Polymorphonuclear cells
100-1000 cells
Reduced glucose (<1/2 plasma)
Raised protein (>1.5)
Bacterial meningitis
CSF:
Fibrin web appearance
Lympho/monoculear
10-1000 cells
Reduced glucose (<1/2 plasma)
Raised protein (1-5)
TB meningitis
Clear CSF
Lympho/monoculear
50-1000 cells
>1/2 plasma glucose
Mild raised protein (<1)
Viral meningitis
Sudden onset, worst ever occipital headache
Meningisim, focal signs, reduced conciousness
?SAH
SAH
Dense material in the basal cisterns and fissures is due to acute bleeding into the subarachnoid space
Blood in the subarachnoid space can fill or partly fill the sulci, fissures, basal cisterns and ventricles
Blood in the ventricles may be the only sign of subarachnoid haemorrhage
When a CT scan is acquired the patient lies supine and any blood in the lateral ventricles will collect posteriorly
Calcification of the choroid plexus is a normal finding which should not be mistaken for intraventricular blood
Headache, vomiting, seizures, vision, papilloedema
Saggital venous sinus thrombosis
Headache +/- mastoid pain, focal CNS signs, seizures, papilloedema
Transverse venous sinus thrombosis
?Venous sinus thrombosis
MRV
Thunderclap headache
Stroke-like focal symptoms over days
Focal seizures common
Cortical vein thrombosis
Def: CVST
Cerebral venous sinus thrombosis (CVST) is the presence of acute thrombosis (a blood clot) in the dural venous sinuses, which drain blood from the brain. Symptoms may include headache, abnormal vision, any of the symptoms of stroke such as weakness of the face and limbs on one side of the body, and seizures. The diagnosis is usually by computed tomography (CT/CAT scan) or magnetic resonance imaging (MRI) employing radiocontrast to demonstrate obstruction of the venous sinuses by thrombus.[1]
Treatment is with anticoagulants (medication that suppresses blood clotting), and rarely thrombolysis (enzymatic destruction of the blood clot). Given that there is usually an underlying cause for the disease, tests may be performed to look for these. The disease may be complicated by raised intracranial pressure, which may warrant surgical intervention such as the placement of a shunt.
Fever, photophobia, neck stiffness, Kernig’s +ve
Purpuric rash
Reduced consciousness
Meningitis
Fever, odd behaviour, fits, focal neurology, reduced consciousness
Encephalitis
Constant unilateral eye pain radiating to forehead
Reduced acuity, haloes, N+V
Red eye, cloudy cornea
Dilated, non-responsive pupil
Acute glaucoma
Bilateral/vertex-bitermopral non-pulsatile band-like headache
Tension headache
Unilateral throbbing
N+V, phono/photophobia
Prodrome->aura-> headache
Migraine
Rapid onset, very severe pain around/behind one eye
Red, watery eye, nasal congestion
Miosis, ptosis
Attacks lasting 15mins-3hrs 1-2x/day mostly nocturnal
Episodes last 4-12w, can be chronic or episodic
Cluster headaches
Rx in cluster headache
?Neuroimaging- GP/neurologist discussion
Acute:
Subcutaenous or nasal triptan: e.g. subcut sumatriptan 6mg (most rapid and effective)
Arrange provsiion of home and ambulatory oxygen therapy: 100% O2 at 12l per minute via a non-rebreathe mask and a reservoir bag
(Do not offer paracetamol, aspirin, NSAIDs, or oral triptans for acute treatment)
Prophylactic: verapamil
Acute Rx in cluster headache
Subcut/nasal triptan
100% O2
Cluster headache prophlyaxis
Verpamail
Paroxysmal hemicranias
Cluster-like headache lasting 5-45 mins 5-30 times/day
SUNCT
Short-lasting unilateral neuralgia with conjunctival injection and tearing, attacks last 15-60s, recure 5-30x/hr
Hemicrania continua
Continuous cluster-like headache
Rx of hemicranias
All repsond well to indomethacin
Paroxysms of unilateral intense stabbing pain in trigeminal distribution
Triggered by washing area, shaving, eating talking
Male >50y
Trigeminal neuralgia
What is significant in trigeminal neuralgia
2o in 14%:
Compression of CNV
MS
Zoster
Chiari malformation
Ix in trigeminal neuralgia
Ix: exclude 2o cause with MRI
Rx in trigeminal neuralgia
Carbamazepine (100mg BD and titrate slowly)
Specialist involvement if doesn’t work (Lamotrigine and gabapentin are alternatives)
Surgical: microvascular decompression
Episodic headache becoming daily chronic headache
Using OTC analgesia >6d/m
Analgesia overuse
Headache worse in morning, stooping, visual problems, obese woman
Raised ICP headache
Headache worse when sitting or standing
Reduced ICP headache
Preauricular pain on chewing
Associated with crepitus
Earache, headache
TMJ dysfunction
GCA
rule of 60
>60y
ESR >60
pred 60mg
Unilateral temple/scalp pain and tenderness
thcikened, pulseless temporal artery
Jaw claudication, amaurosis fugax, sudden blindness
Associated with PMR in 50%
GCA
Ix in GCA
ESR +++
Raised plt
Raised ALP
Reduced Hb
Temporal artery biopsy
Rx in GCA
High dose prednisolone (60mg/d PO) for 5-7d
Opthalmology involvement
Guided by symptoms and ESR
Give PPI and bisphosphonate
Start 75mg OD aspirin
Steroid dose is gradually tapered over 1-2y with most patients reaching complete remission
Epidemiology of migraine
8% prevalence
F>M
RFs Migraine
Obesity
PFO
Pathophysiology of migraine
Vascular: cerebrovascular constriction-> aura, dilatation -> headache
Brain: spreading cortical depression
Inflammation: activation of CNV nerve terminals in the meninges and cerebral vessels
Migraine triggers
CHOCOLATE
Cheese
OCP
Caffeine
alcohOL
Anxiety
Travel
Exercise
Symptoms of migraine
Headache
Prodrome (50%)
Aura (20%)
How can migraine be classified
With aura (classical migraine)
Without aura (common migraine)
Features of migraine headache
Aura lasting 15-30 mins then unilateral, throbbing headache
Phono/photophobia
Nausea/vomiting
Allodynia
Often premenstrual
Features of migraine prodrome
50%
Precede migraine by hours-days
Yawnings
Food cravings
Changes in sleep, appetite or mood
Features of migraine aura
20%
Precedes migraine by minutes and may persist
Vsiual: distortion, lines, dots, zig-zags, scotoma, hemianopia
Sensory: paraesthesia (fingers-> face)
Motor: dysarthria, ataxia, ophthalmoplegia, hemiparesis (hemiplegic migraine)
Speech: dysphasia, paraphasia
Diagnostic criteria for migraine
Typical aura and headache or
>5 headaches lasting 4-72h with either n/v or photo/phonophobia and >2 of:
unilateral
pulsating
interferes with normal life
worsened by routine activity
DDx migraine
Cluster/tension headache
Cervical spondylosis
HTN
Intracranial pathology
Epilepsy
Acute management of migraine
1st line- combination therapy
Oral triptan e.g. (sumatriptan 50/100mg) and an NSAID e.g. ibuprofen
or an oral triptan and paracetamol
If monotherapy preferred consider oral triptan, NSAID or aspirin (900mg every 4-6h) or paracetamol
Consider adding an anti-emetic e.g. metoclopramide, domperidone, prochlorperazine even in the absence of N+V
Preventative treatment of migraine
1st line
Topiramate or propranolol
2nd line
Amitryptilline
3
Acupuncture
Riboflavin may be effective in reducing migraine frequency and intensity
NB re Topiramate in pregnancy
Assoicated with fetal malformations and can impair hormonal contraception
Epidemiology of SAH
9/100,000
35-65yrs
Causes of SAH
Rupture of saccular aneurysms (80%)
AVMs (15%)
RFs for SAH
Smoking
HTN
EtOH
Bleeding diathesis
Mycotic aneurysms (bacterial infection of arterial wall- SBE)
FHx (close relatives have 3-5x risk
What are the sites of Berry Aneurysms
Junction of posterior communicating with IC
Junction of anterior communicating with ACA
Bifurcation of MCA
What conditions are associated with SAH?
Adult PKD
Coarctation of the aorta
Ehlers Danlos
Sudden severe occipital headache
Collapse
Meningism: neck stiffnes, N/V, photophobia
Seizures
Drowsiness-> coma
?SAH
Sentinal headche
6% of SAH patients experience sentinal headache from small warning bleed
Signs of SAH
Kernig’s
Retinal or subhyaloid haemorrahge
Focal neurology: at presentation suggests aneurysm location, later deficits suggest complications
Kernig’s sign
Kernig’s sign. Kernig’s sign (after Waldemar Kernig (1840–1917), a Russian neurologist) is positive when the thigh is flexed at the hip and knee at 90 degree angles, and subsequent extension in the knee is painful (leading to resistance). This may indicate subarachnoid hemorrhage or meningitis.
Brudzinski’s sign
Jozef Brudzinski (1874–1917), a Polish pediatrician, is credited with several signs in meningitis. The most commonly used sign (Brudzinski’s neck sign) is the appearance of involuntary lifting of the legs when lifting a patient’s head off the examining couch, with the patient lying supine.
DDx for SAH
In 1o care, 25% of those with thunderclap headache have SAH
50-60% have no cause found
Rest: meningitis, intracerebral bleeds, cortical vein thrombosis
Ix of SAH
CT
LP
CT sensitivity in SAH
Detects >90% of SAH within first 48h
LP in SAH
If CT -ve and no CIs, >12h after start of headache
Xanthochromia due to break down of bilirubin
Mx of SAH
Frequent neuro obs: pupils, GCS, BP
Maintain cerebral perfusion pressure, keep SBP >160
Nimodipine for 3w (reduces cerebral vasopsasm)
Endovascular coiling (preferable to surgical clipping
Complications of SAH
Rebleeding (20%): commonest cause of mortality
Cerebral ischaemia: due to vasospasm: commonest cause of morbidity
Hydrocephalus: due to blockage of arachnoid granulations, may require ventricular or lumbar drain
Hyponatraemia: dont Mx with fluid restriction
Mx of saccular aneruysm
Young patients with aneurysms >7mm in diameter may benefit from Sx
Def: stroke
Rapid onset, focal neurological deficit due to a vascular lesion lasting >24h
Pathogenesis of stroke
Infarction due to ischaemia (80%)
or intracerebral haemorrhage (20%)
Parthophysiology of ischaemic stroke
Atheroma: large e.g. MCA
Small vessel perforators (lacunar)
Pathophysiology of embolic stroke
Cardiac (30% of strokes): AF, endocarditis, MI
Atherothromboembolism e.g. from carotids
Aetiology of haemorrhagic stroke
Raised BP
Trauma
Aneurysm rupture
Anticoagulation
Thrombolysis
Rarer causes of stroke
Watershed stroke: sudden reduction in BP e.g. sepsis
Carotid artery dissection
Vasculitis: PAN, HIV
Cerebral vasospasm 2o to SAH
Venous sinus thrombosis
Anti-phospholipid syndrome, thromobphilia
RFs for stroke
HTN
Smoking
DM
Raised lipids
FHx
Cardiac: AF, valvular disase
Peripheral vascular disease
Previous Hx
Ethnicity: raised in blacks and asians
Raised PCT/Hct
OCP
Cardiac causes of stroke
AF: 4.5%/y
External cardioversion: 1-3%
Prosthetic valves
Acute MI esp. large anterior
Paradoxical systemic emboli
Cardiac sx
Valve vegetations
Ix in determining cause of stroke
ID risk factors for further strokes:
HTN
Cardiac emobli
Carotid artery stenosis
Bleeding/thrombotic tendency
Hyperviscosity
Metabolic
Vasculitis
Identifying aetiology of stroke:
HTN
Retinopathy
Nephropathy
Big heart on CXR
Identifying aetiology of stroke:
Cardiac emboli
ECG +/- 24hr tape for AF
Echo: mural thrombus, hypokinesis, valve lesions, ASD, VSD
Identifying aetiology of stroke:
Cartoid artery stenosis
Doppler US +/- angio
Endarterectomy beneficial if >70% symptomatic stenosis
When is endarterectomy beneficial in context of carotid artery stenosis?
If >70% symptomatic stenosis
Identifying aetiology of stroke:
Bleeding/thrombotic tendency
Thrombophilia screen
Thrombocytopenia
Identifying aetiology of stroke:
Hyperviscosity
PCV
SCD
Myeloma
Identifying aetiology of stroke:
Metabolic
Glucose
Lipids
Hyperhomocystinaemia
Identifying aetiology of stroke:
Vasculitis
Raised ESR
ANA
What is used to classify Stroke?
Oxford/Bamford classification
Based on clinical localisation of inffarct
S= syndrome: prior to imaging
I= infarct after imaging when atheroembolic infarct confirmed
TACS=
Total anterior circulation stroke
What arterial territory involved in TACS?
Large infarct in carotid/ MCA, ACA territory
Clinical features of TACS
All 3 of:
- Hemiparesis (contralateral) and/or sensory deficit (>2 of face, arm and leg)
- Homonymous hemianopia (contralateral)
- Higher cortical dysfunction
- Dominant (L usually): dysphasia
- Non-dominant: hemispatial neglect
All 3 of:
- Hemiparesis (contralateral) and/or sensory deficit (>2 of face, arm and leg)
- Homonymous hemianopia (contralateral)
- Higher cortical dysfunction
- Dominant (L usually): dysphasia
- Non-dominant: hemispatial neglect
TACS
PACS=
Partial anterior circulation syndrome
Territory affected by PACS?
Carotid/MCA and ACA territory
Clinical features of PACS
2/3 of TACS criteria, usually:
- Hemiparesis (contralateral) and or sensory deficit
- Higher cortical dysfunction
Dominant: dysphasia
Non-dominant: neglect, constructional apraxia
Deficit is less dense and/or incomplete
2/3 of TACS criteria, usually:
- Hemiparesis (contralateral) and or sensory deficit
- Higher cortical dysfunction
Dominant: dysphasia
Non-dominant: neglect, constructional apraxia
Deficit is less dense and/or incomplete
PACS
POCS=
Arterial territory affected?
Posterior circulation stroke
Infarct in vertebrobasilar territory
Clinical features of POCS?
Cerebellar syndrome
Brainstem syndrome
Contralateral homonoymous hemianopia
LACS
Arterial territory affected?
Lacunar stroke
Small infarcts around basal ganglia, internal capsule, thalamus and pons
What is there an absence of in LACS?
Higher cortical dysfunction
Homonymous hemianopia
Drowsiness
Brainstem signs
What are the 5 LACS syndromes?
Pure motor: posterior limb of internal capsule- commonest
Pure sensory: posterior thalamus (VPL)
Mixed sensorimotor: internal capsule
Dysarthria/clumsy hand
Ataxic hemiparesis: anterior limb of internal capsule, weakness and dysmetria
Ischaemic pointers in stroke
Carotid bruit
AF
Past TIA
IHD
Haemorrhagic pointers in stroke
Meningism
Severe headache
Coma
Brainstem infarcts, clinical features
Complex signs depending on relationship of infarct to CN nuclei, long tracts and brainstem connections
Brainstem infarct, region affected
Hemi/quadraparesis
Corticospinal tracts
Brainstem infarct, region affected
Conjugate gaze palsy
Oculomotor system
Brainstem infarct, region affected
Horner’s syndrome
Sympathetic fibres
Brainstem infarct, region affected
Facial weakness (LMN)
CN7 nucleus
Brainstem infarct, region affected
Nystagmus, vertigo
CN8 nucleus
Brainstem infarct, region affected
Dysphagia, dysarthria
CN9 and 10
Brainstem infarct, region affected
Dysarthria, ataxia
Cerebellar connections
Brainstem infarct, region affected
Reduced GCS
Reticular activating system
Which artery affected in LMS/ Wallenberg’s syndrome
PICA or vertebral artery
Features of LMS/ Wallenberg’s syndrome
DANVAH
Dysphagia
Ataxia
Nystagmus
Vertigo
Anaesthesia: ipsilateral facial numbness and absent corneal reflex, contralateral pain loss
Horner’s syndrome
Features of Millard-Gubler syndrome
Pontine infarct
6th and 7th CN nuclei + corticospinal tracts:
Diplopia
LMN facial palsy and loss of corneal reflex
Contralateral hemiplegia
DDx for stroke
Head injury +/- haemorrhage
Glucose derangement
SOL
Hemiplegic migraine
Todd’s palsy
Infections: encephalitis, abscesses, Toxo, HIV, HTLV
Drugs e.g. opiate overdose
Acute management of stoke
Resuscitate
Monitor
Imaging
Medical
Surgical
Stroke Unit
Secondary prevention
Rehabilitation
Resuscitation in stroke
ABC
Ensure patent airway: consider NGT
NBM until swallowing assessed by SALT
Don’t overhydrate: risk of cerebral oedema
Monitoring in acute mx of stroke
Glucose: 4-11mM: sliding scale if DM
BP <185/110 for thrombolysis NB Rx of HTN can reduce cerebral perfusion
Neuro obs
Imaging in acute stroke
Urgent CT/MRI
CT used to exclude 1o haemorrhage
Diffusion-weighted MRI is most sensitive for acute infarct
Medical management of stroke
Consider thrombolysis if 18-80 years and <4.5hrs since onset of symptoms
Alteplase
CT 24h post thrombolysis to look for haemorrhage
Aspirin 300mg PO/PR once haemorrhagic stroke excluded +/- PPI, clopidogrel if aspirin sensitive
Cerebral perfusion pressure
(CPP) = MAP – ICP or CVP (whichever is highest)
Surgical Mx of stroke
Neurosurgical opinion if ICH
May coil bleeding aneurysms
Decompressive hemicraniectomy for some forms of MCA infarction
Features of stroke unit
Specialist nursing and physio
Early mobilisation
DVT prophylaxis
1o prevention of stroke
Control RFs: HTN, lipids, DM, smoking, cardiac disease
Conisder life long anticoagulation in AF (use CHADS2)
Cartoid endarterectomy if symptomatic 70% stenosis
Exercise
Secondary prevention of stroke
Risk factor control as for primary prevention, start a statin after 48h
Aspirin/clopidogrel 300mg for 2w after stroke then either
clopidogrel 75mg OD (preferred option)
Aspirin 75mg OD + dipyridamole MR 200mg BD
Warfarin instead of aspirin/clopidogrel if cardioembolic stroke or chronic AF, start from 2w post-stroke. Don’t use aspirin and warfarin together
Carotid endarterectomy if good recovery and ipsilateral stenosis
Features of post-stroke rehab
MENDS
MDT: physio, SALT, dietician, OT, specialist nurses, neurologist, family
Eating: screen swallowing: NG/PEG if unable to take. Screen for malnutrition (MUST tool)
Neurorehab: physio and speech therapy
DVT prophylaxis
Sores: must be avoided at all costs
MUST tool
‘MUST’ is a five-step screening tool to identify
adults,
who are malnourished, at risk of malnutrition
(undernutrition), or obese. It also includes management guidelines which can be used to develop
a care plan.
OT purpose
Impairment: paralysed arm
Disability: inability to write
Handicap: can’t work as accountant
OT aims to minimise diability and abolish handicap
Px stroke
10% recurrence
Px PACS
20% mortality
1/3 survivors independent
2/3 of survivors dependents
Px TACS
60% mortality
5% independance
Def: TIA
Sudden onset focal neurology lasting <24h due to temprorary occlusion of part of the cerebral circulation
~15% of strokes are preceded by TIAs
Symptoms usually brief
Global evenets e.g. syncope/dizziness are not typical
Signs mimic those of CVA in the same arterial territory
TIA
Signs of causes of TIA
Carotid bruits
Raised BP
Heart murmur
AF
Causes of TIA
Atherothromboembolism from carotids is the main cause
Cardioembolism: Post-MI, AF, valve disease
Hyperviscosity: polycytheamia, SCD, myeloma
DDx for TIA
Vascular: CVA, migraine, GCA
Epilepsy
Hyperventilation
Hypoglycaemia
Ix in TIA
Aim: to find cause and define vascular risk
Bloods: FBC, U&E, ESR, glucose, lipids
CXR
ECG
Echo
Carotid doppler +/- angiography
Consider diffusion weighted MRI
Mx of TIA time to intervention
Intervention within 72h-> 2% strokes @90d
Intervention within 3w: 10% strokes @90d
Mx of TIA
ACAS
Antiplatelet therpay/anticoagulate
Cardiac risk factor control
Assess risk of subsequent stroke
Speciliast referral to TIA clinic
Antiplatelet/anticoaglant therapy in TIA
Aspirin/clopidogrel 300mg/d for 2w then 75mg/d, add dipridamole MR to aspirin
Clopidogrel preferred for LT
Warfarin if cardiac emboli: AF, MI, MS- after 2wks
How is risk of stroke subsequent to TIA assessed?
ABCD2 score
Px of TIA
Combined risk of stroke and MI is 9%/year
3x increased in mortality in comparison to TIA free populations
Components of ABCD2 score
Age >60
BP >140/90
Clinical features: unilateral weakness (2 points), speech disturbance without weakness (1)
Duration:
>1h (2 points)
10-59 mins (1 point)
DM
Maximum of 7 points
Score cut offs for ABCD2
Score >4-> TIA clinical within 24hours
Score <4: TIA clinic within 1w
ABCD2 prognosis
Score >6: 8% risk of stroke within 2d, 35% risk within 1w
Score >4
All patients with suspected TIA should be seen by specialist within 1w
Def: SDH
Bleeding from bridging veins between cortex and sinuses
Haematoma between dura and arachnoid
Often due to minor trauma that occured a long time previously- especially deceleration injuries
Bleeding from bridging veins between cortex and sinuses
Haematoma between dura and arachnoid
Often due to minor trauma that occured a long time previously- especially deceleration injuries
SDH
RFs for SDH
Elderly: brain atrophy
Falls: epileptics, alcoholics
Anticoagulation
Headache
Fluctuating GCS, sleepiness
Gradual physical or mental slowing
Unsteadiness
?SDH
Signs in SDH
Raised ICP can lead to tentorial herniation
Localising signs occur late
CT/MRI findings in SDH
Crescenteric heamatoma over one hemisphere
Clot goes from white-> grey with time
Mid-line shift
Crescenteric heamatoma over one hemisphere
Clot goes from white-> grey with time
Mid-line shift
?SDH
SDH
Mx of SDH
1st line: irrigation/evacuation via burr-hole craniostomy
2nd line: craniotomy
Address causes of trama
DDx SDH
Stroke
Dementia
SOL
Def: EDH
Often due to # temporal or parietal bone leading to MMA and vein laceration
Blood between bone and dura
Suspect if after head inury GCS falls, is slow to improve or there is a lucid interval
Deterioration of GCS after head injury that caused no LOC or following initial improvements in GCS
Can last hrs or days
EDH
Lucid Interval
Symptoms of raised ICP
Brainstem compression
?EDH
Headache
Vomiting
Confusion-> coma
Fits
Ipsilateral blown pupil (surgical 3rd nerve palsy)
+/- hemiparesis with upgoing plantars and reflexes
?Raised ICP
Symptoms of brainstem compresion?
Deep irregular breathing
Cushing response: raised BP, reduced HR is late
Death by cardiorespiratory arrest
Lens-shaped haematoma
Skull #
?EDH
Mx of EDH
Neuroprotective ventilation: O2 >100, Co2 35-40
Consider mannitol (1g/kg IV via central line)
Craniectomy for clot evacuation and vessel ligation
EDH
Features of intracranial venous thrombosis
Symptoms come on gradually over days-weeks
Sinus thrombosis may extend into cortical veins
Types of intracranial dural venous sinus thrombosis
Saggital sinus
Transverse
Sigmoid
Inferior petrosal
Cavernous sinus
Features of saggital sinus thrombosis
45% of IVT
Often co-exists if other sinuses are thrombosed
Headache, vomiting, seizures, altered vision, papilloedema
Features of transverse sinus thrombosis
35% of IVT
Headache +/- mastoid pain, focal neurology, seizures, papilloedema
Features of sigmoid sinus thrombosis
Cerebellar signs
Lower CN palsies
Features of inferior petrosal sinus thrombosis
5th and 6th CN palsies
Gradenigo’s syndrome
Gradenigo’s syndrome, also called Gradenigo-Lannois syndrome[1][2] and petrous apicitis, is a complication of otitis mediaand mastoiditis involving the apex of the petrous temporal bone. It was first described by Giuseppe Gradenigo in 1904 when he reported a triad of symptoms consisting of periorbital unilateral pain related to trigeminal nerve involvement, diplopia due to sixth nerve palsy and persistent otorrhea, associated with bacterial otitis media with apex involvement of the petrous part of the temporal bone (petrositis). The classical syndrome related to otitis media has become very rare after the antibiotic era.
Symptoms[edit]
Features of cavernous sinus thrombosis
Spread from facial pustules of folliculitis
Headache, chemosis, eyelid oedema, proptosis, painful opthalmoplegia, fever
Often-> venous infarcts with stroke-like focal symptoms evolving over days
Thunderclap headache
Focal seizures
?Cortical vein thrombosis
DDx for intracranial venous thrombosis
SAH
Meningitis
Encephalitis
Intracranial abscess
Arterial stroke
Common causes of intracranial venous thrombosis
Pregnancy/puerperium
OCP
Head injury
Dehydration
Intracranial/extracranial malignancy
Thrombophilia
Ix in intracranial venous thrombosis
Exclude SAH and meningitis
CT/MRI venography: absence of a sinus
LP: raised pressure, may show RBCs and xanthochromia
Mx of intracranial venous thrombosis
LMWH-> warfarin (INR 2-3)
Fibrinolytics e.g. streptokinase can be used via selective catheterisation
Thrombophilia screen
Outline the features of the dural venous sinuses
Lie between the periosteal and meningeal layers of the dura mater
All ultimately drain into the internal jugular vein.
11 sinuses in total.
Straight, superior and inferior saggital sinuses are found in the falx cerebri of the dura mater. They converge at the confluence of sinuses (overlyling the internal occipital protruberance).
The straight sinus is a continuation of the great cerebral vein and the inferior sagittal sinus.
From the confluence, the transverse sinus continues bilaterally and curves into the sigmoid sinus to meet the opening of the IJV
Cavernous sinus drains the ophthalmic veins and is found either side of the sella turcica.
Blood returns to the IJV via the superior or inferior petrosal sinuses.
What is Trolard?
The superior anastomotic vein that connects the superficial middle cerebral vein to the superior sagittal sinus
What is the Labbe
Connects the superficial middle cerebral vein to the transverse sinus
What is the vein of Galen?
The great cerebral vein
Who was Galen
Aelius Galenus or Claudius Galenus (/ɡəˈliːnəs/;[1] Greek: Κλαύδιος Γαληνός; September 129 AD – c. 200/c. 216), often Anglicized as Galenand better known as Galen of Pergamon (/ˈɡeɪlən/),[2] was a prominentGreek physician, surgeon and philosopher in the Roman Empire.[3][4][5]Arguably the most accomplished of all medical researchers of antiquity, Galen influenced the development of various scientific disciplines, including anatomy,[6] physiology, pathology,[7] pharmacology,[8] andneurology, as well as philosophy[9] and logic.
Vein of Galen
How can the features of meningitis be classified?
Meningitic
Neurological
Septic
Meningitic features
Headache
Neck stiffness: Kernig’s and Brudzinski’s
Photophobia
N+V
Neurological features of meningitis?
Reduced GCS-> coma
Seizures (20%)
Focal neurology (20%) e.g. CN palsies
Clinically septic
Fever
Reduced BP, Increaed HR
Increased CRT
(purpuric rash)
DIC
Abx management of meningitis in the community
Admit to hospital as emergency
IM benzylpenicillin 1200mg Adults dose
Children <1y meningitis in the community benpen dose
300mg
Children <10 >1 meningitis in community benpen dose
600mg
Adult/children >10 meninigits in the community, benpen dose
1200mg
Abx therapy in hospital meningitis
<50
Ceftriaxone 2g IVI/IM BD
Abx therapy in hospital setting meningitis
>50
Ceftriaxone and ampicillin 2g IVI/4h
Viral causes of meningitis
Enteroviruses (coxsackie, echovirus)
HSV2
If ?HSV meningitis
Aciclovir
Bacterial causes of meningitis
Meningococcus
Pneumococcus
Listeria
Haemophilus
TB
Cryptococcus
Sepsis 6
Administer high flow O2 to maintain target O2 saturations greater than 94%
Take blood cultures
Give IV Abx
Start IV fluid resuscitation (fluid bolus)
Check lactate
Monitor UO
Mx of mainly septicaemic meningococcal infection
Don’t attempt LP
Ceftriaxone 2g IVI
Consider ITU if shocked
Mx of mainly meningitic meningococcal infection
If no shock or CIs- LP
Dexamethasone 0.15mg/kg IV QDS
Ceftriaxone 2g IVI post-LP
Continuing management of meningitis
Ceftriaxone 2g BD IVI
Meningococcus: 7d IV then review
Pneumoccus: 14d IV then review
Maintenance fluids:
UO >30ml/h
SBP >80mmHg
If response is poor consider intubation +/- inotropic support
Rifampicin prophylaxis for household contacts
Contraindications to LP
Try LP Unless ContraINdicated
Thrombocytopenia
Lateness (i.e. delaying Abx administration)
Pressure (signs of raised ICP)
Unstable (cardio and respiratory systems)
Coagulation disorder
Infection at LP site
Neurology (focal neurological signs)
Infectious prodrome: fever, rash, LNs, cold sores, conjunctivitis, meningeal signs
Bizzare behaviour or personality change
Confusion
Reduced GCS-> coma
Fever
Headache
Focal neurology
Seizures
Hx of travel or animal bite
?Encephalitis
Viral causes of encephalitis
HSV 1.2
CMV, EBV, VZV
Arboviruses
HIV
Ix for causes of encephalitis
Bloods: cultures, viral PCR, malaria film
Contrast CT: focal bilateral temporal involement suggests HSV
LP: raised CSF proteins, lymphocytes, PCR
EEG: shows diffuse abnormalities, may confirm Dx
Encephalitis with focal bilateral temporal involvement on contrast CT
Suggests HSV encephalitis
Ix in meningitis
Bloods: FBC, U+Es, clotting, glucose, ABG
Blood cultures
LP: MCS, glucose, virology/PCR, lactate
Mx of encephalitis
Aciclovir STAT: 10mg/kg/8h IV over 1h for 14/7
Supportive measures in HDU/ITU
Phenytoin for seizure control
Encephalitic symptoms without fever, consider
Encephalopathy
Causes of encephalopathy (non-infective)
Reduced glucose
Hepatic
DKA
Drugs
SLE
Uraemia
Hypoxic brain injury
Beri-Beri
Pre-disposing factors to cerebral abscess