2. Learning objectives
0 Anatomical language
0 The main bones of the skull
0 External and internal (sagittal) view of the brain
0 The forebrain, midbrain and hindbrain
0 The Circle of Willis

3. Anatomical language for the
brain
Before we go any further however, let’s go through the
basics…
Anatomy of the brain comes with its own weird and
wonderful language. Understanding the anatomy of the
brain becomes a lot easier as soon as you understand
the language that comes with it.

4. Anatomical language for the
brainrostra means
beak/nose, so
Rostral means
closer to the nose
Cauda means tail
(ie cauda equina),
so
Caudal means
closer to the
spine

5. Anatomical Language for the
brain0 The brain is folded into
Gyri and sulci
0 Gyri (singular gyrus) are
the raised bumps of the
folds
0 Sulci (singular sulcus)
are the grooves between
the folds
0 The longitudinal fissure
(aka the median fissure)
splits the two halves of
the cerebrum

6. Anatomical language for the
brain
0 Grey Matter is matter
composed of unmyelinated
neuron bodies, neurons and
glial cells
0 White matter is matter
composed of myelinated axons
and glial cells and is the lipid
content of the myelin sheaths
that makes this area appear
white

7. Anatomical language for the
brain
There are 3 layers covering the
brain:
0 The dura mater is the outermost
layer. As its name might suggest its
very durable and coats the whole
of the brain and spinal cord in one
continuous sheath
0 The arachnoid mater is the middle
layer. All cerebral veins, arteries
and cranial nerves lie beneath this
layer in an area known as the
subarachnoid space
0 The pia mater is a vascular
membrane that intimately covers
all gyri and sulci of the brain

8. The Skull
A quick revision of the main bones of the skull

9. A brief overview of the brain
External Structures
Cerebrum
Cerebellum
brainstem
Pons
Medulla

10. A Brief Overview of the Brain
Internal Structures
Sagittal section of
the brain

11. Functional areas of the brain
The brain is grouped into 3 areas
based loosely on embryological
formation:
0 The Forebrain – cerebrum and
the diencephalon
0 The Midbrain –tegmentum and
tectum
0 The Hindbrain – cerebellum,
medulla oblongata and pons

12. The forebrain
The cerebrum
0 Also known as the telencephalon
0 Thought to be the seat of humanity
as its so well developed in humans
0 Composed of two hemispheres
(left and right) divided by the
median fissure
0 Commissures (tracts of axons
crossing the midline) connect
these two hemispheres, the largest
of which is the corpus callosum
0 Covered in a 2-4mm thick layer of
grey matter - the cerebral cortex

13. Lobes of the Cerebrum
0 The lobes of
the cerebrum
are described
in terms of the
skull bones
they lie behind

14. The cerebrum
Functions of the cerebral cortex include:
0 Sensory perception
0 Memory
0 Planning/execution of voluntary movement
0 Language
0 Consciousness
0 Self Awareness
0 Cognitive functions

15. The cerebrum
Brodmann’s map divides the cerebral cortex into 52
different functional areas that are either motor, sensory
or associational.

16. The forebrain
The diencephalon
Composed of the
hypothalamus, thalamus,
epithalamus and subthalamus
The hypothalamus:
0 thermoregulation and
triggering sleep
0 part of the limbic system
(generates goal directed
behaviours - eating, drinking
etc.)
0 Controls many endocrine
functions via connections to
the pituitary gland

17. The forebrain
The diencephalon
The Epithalamus:
0 Regulates circadian rhythm
0 Contains the pineal gland
The Thalamus has multiple
functions:
0 Emotion (limbic system)
0 Memory (frontal cortex)
0 Sensory and motor
0 Pain and visual attention
0 Sleep/wakefulness and arousal
The Subthalamus is involved in
movement

18. The Midbrain
The mesencephalon
2 parts:
0 Tegmentum - receives
cranial nerves III – V
and contains substantia
nigra
0 Tectum – receives
cranial nerves II and
VIII; mediates
visual/auditory reflexes

19. The hindbrain
The Cerebellum
Makes up ¼ brain mass and ½
the brain’s total neurons
Cortex is composed of grey
matter folded into folia
separated by transverse
fissures
White matter is called arbor
vitae “tree of life”
Concerned with high level
functions:
0 timing and execution of a
voluntary movement
0 Learning new motor skills
0 Cognition

20. The hindbrain
Pons and Medulla Oblongata
The centres for life support functions of the brain
0 Pons consists mainly of nerve fibres connecting the
cerebellar hemispheres, forebrain, midbrain and
spinal cord
0 Medulla consists of 2 pyramids separated by a median
fissure
0 Descending fibres cross from left to right in the
medulla, known as the decussation of the pyramids

21. The Circle of Willis
0 Circle of Willis is meant
to be the brain’s
insurance mechanism
against arterial
blockages which could
cause CVAs
0 If one artery is blocked
other arteries in the
circle can compensate to
continue supplying the
affected area with blood
0 In reality the circle of
Willis is often too small
to be effective and isn’t
really able to cope with
large scale CVAs

22. The Circle of Willis
0 The Internal Carotid
arteries and the
vertebral arteries
form the main blood
supply
0 They meet in the
middle via the two
posterior
communicating
arteries and the
basilar artery
The basilar and
vertebral arteries
supply the brainstem
Internal Carotid arteries
Vertebral arteries
Posterior communicating artery
Basilar artery

23. Internal Carotid arteries
Vertebral arteries
Posterior communicating artery
Basilar artery
The Circle of Willis
The Internal carotids
branch form the anterior
cerebral arteries. these
supply:
0 the medial surface of the
frontal and parietal lobes
0 1 inch of brain either side
of the median fissure
0 Occlusion can damage
motor nuclei cranial
nerves V, VII and XII
affecting movement of
jaw, lips and tongue
respectively
The Anterior
communicating artery links
the 2 anterior cerbral
arteries
Anterior cerebral arteriesAnterior
communicating
artery

24. Internal Carotid arteries
Vertebral arteries
Posterior communicating artery
Basilar artery
The Circle of Willis
0 Middle cerebral
arteries supply lateral
parts of cerebral
hemispheres except
occipital and inferior
temporal lobe
0 Anterior choroidal
arteries supply
thalamus and
hypothalamus and
various important
forebrain groups
Anterior cerebral arteryAnterior
communicating
artery
Middle cerebral artery
Anterior choroidal artery

25. Internal Carotid arteries
Vertebral arteries
Posterior communicating artery
Basilar artery
The Circle of Willis
Posterior cerebral
arteries supply:
0 Occipital lobe
0 Inferior temporal lobe
0 Midbrain
Superior and inferior
cerebellar arteries
supply:
0 Pons
0 Medulla
0 Cerebellum
Pontine arteries supply
medial parts of pons
and medulla
Anterior cerebral arteryAnterior
communicating
artery
Middle cerebral artery
Posterior cerebral artery
Superior cerebellar artery
Inferior cerebellar artery
Pontine
arteries

26. Summary
The brain has a 3 layer covering which allows it to be
suspended in CSF
The brain is divided anatomically into many different areas.
It is composed of three functional parts:
0 The Forebrain – higher functions and endocrine regulation
0 The Midbrain – cranial nerves and substantia nigra
0 The Hindbrain – coordination, movement and life support
functions
The circle of Willis ensures a high arterial blood supply with
the possibility of compensatory blood supply in a CVA

27. Thank you for your time
0 Any questions?

28. Pathophysiology of a
Cerebrovascular
Accident
By Tim Sale and
Nicola Tribley

29. Aims:
• Define a stroke
• Distinguish between
types
• Explain what goes
wrong

30. A stroke is an acute neurological
deficit, lasting longer than 24 hours.
A Transient Ischaemic Attack (TIA)
is an acute neurological deficit
lasting less than 24 hours.
Definitions:

31. 3rd most common
cause of death in
developed world
More common
in men
25% of patients
die
More likely to
occur in the
morning
More common
in Black
Africans
The Facts…

32. Types of C.V.A...
Ischaemic stroke/ Infarction – 80-90%
Small vessel
Large vessel stenosis
Cardio-embolic
Haemorrhagic – 10-20%
TIA – Transient Ischaemic Attack

33. Large Vessel
Disease
 Also called
Large
vessel
stenosis
 Rupture of
a local
plaque
 Most
common
type

34. Cardio-embolic
Stroke
 Common
embolic source
 Atrial
fibrillation
 Valvular
changes

35. Small Vessel Disease/
Lacunar Infarct0 25% of strokes
0 Infarcts in the deep (perforating) arteries, from
branches of the middle cerebral artery
0 Very localised, lesions (<5mm) are in the deep brain
– lots of important structures!
0 (37% putamen, 16% pons, 14% thalamus and 10%
caudate)
0 Microatheroma (main cause) and Lipohyalinosis
(thickening of arteriolar wall and reduction in
lumen diameter)

36. Haemorrhagic
• Intraparenchymal- 8-13%
of strokes
• Resulting haematoma can
damage surrounding brain
tissue due to increase in
pressure
• Hypertension damage to
vessel walls (most common)
• Anuerysm/ arteriovenous
malformation rupture
• Altered hemostasis
(coagulation disorders)

37. Cellular Changes
↓blood flow =↓O₂
Na˖/K˖ pump fails
(Na˖ accumulates in cell)
H₂O enters cell causing it to swell
Swelling causes ↑intracranial pressure
Further ↓bloodflow

38. Also…
0 High Na˖ causes cells to continually depolarise
=EXCITOTOXICITY
0 ↑Ca2˖ enters cell leading to necrosis and
Inflammation (via cytokine release)
Cells with CBF <10ml/100g tissue/min will die
within minutes of a stroke - the ‘core’
Cells with CBF <25ml/100g tissue/min can
remain viable for several hours - the ‘penumbra’

40. Anterior
Cerebral
Artery

41. Middle
Cerebral
Artery

42. Posterior
Cerebral
Artery

43. Features Anatomy Prognosis
Total Anterior
Circulation
Infarct (15%)
TACI
1. High cerebral
dysfunction
2. Hemanopia
3. Ipsilateral
motor/sensory
deficit
Middle Cerebral Artery
occluded
High mortality
Poor outcome
Partial Anterior
Circulation
Infarct (35%)
PACI
2/3 of TACI features
Middle cerebral artery/
Anterior Cerebral artery
branch occluded
Fair
High chance of recovery
Lacunar
Circulation
Infarct (25%)
LaCI
Motor/ sensory/ataxic
hemipareisis
Occlusion of small,
deep perforating artery
Often good recovery
Posterior
Circulation
Infarct (25%)
PoCI
1.Cranial nerve palsy
2.Contralateral
motor/sensory
deficit/cerebral
deficit/hemanopia
Brain stem/
cerebellum/ occipital
lobe
Good recovery
High reoccurrence
Categorizing strokes

44. Possible causes and differential
diagnosis of cerebro-vascular
accidents
 Zeenat Umerji

45. What is stroke?
A sudden attack of weakness due to an interruption to the flow
of blood to the brain. Usually affects one side of the body.
 Either:
 Ischeamic (50% cerebral hemisphere, 25%
brainstem, 25% lacunar)
 heamorrhagic
 from prolonged reduction of BP
 Varies in severity from a passing weakness/tingling in a limb
(TIA) to profound paralysis, coma or death

46. Causes
 Chief causes:
 Thrombosis
 Atherothromboembolism
 Heart emboli
 CNS bleed (BP increased, trauma, aneurism
rupture)

47. Causes
 Rare causes:
 Vasculitis
 Venus sinus thrombosis
 Young patients:
 Thrombophilia
 Vasculitis subarachnoid haemorrhage
 Venus-sinus thrombosis
 Carotid artery dissection

48. Presentations
 Cerebral hemisphere infarcts: initially flaccid then spastic
contra-lateral hemiplegia, contra-lateral sensory loss,
hemianopia, dysphasia
 Brainstem infarction: quadriplegia (paralysis affecting all four
limbs), disturbances of gaze & vision, locked-in syndrome
 Lacunar infarcts: poor motor/sensory signs, ataxia, intact
cognition/consciousness

49. Differential diagnosis
 CNS tumour
 Subdural haemorrhage
 Seizure (Todd's palsy)
 Hypoglycaemia
 Hyperglycemia
 Drug overdose (if comatose)
 Meningitis
 Migraine

50. Differential diagnosis
 CNS tumour
 Subdural haemorrhage
 Seizure (Todd's palsy)
 Hypoglycaemia
 Hyperglycemia
 Drug overdose (if comatose)
 Meningitis
 Migraine
Altered
consciousness
Hemiparesis
Signs of trauma

51. Differential diagnosis
 CNS tumour
 Subdural haemorrhage
 Seizure (Todd's palsy)
 Hypoglycaemia
 Hyperglycemia
 Drug overdose (if comatose)
 Meningitis
 Migraine
Altered consciousness
Hemiparesis (Todd's paralysis)
History of seizures
Seizure medication

52. Differential diagnosis
 CNS tumour
 Subdural haemorrhage
 Seizure (Todd's palsy)
 Hypoglycaemia
 Hyperglycemia
 Drug overdose (if comatose)
 Meningitis
 Migraine
When glucose is ≤50 or ≥300
Altered consciousness
Hemiparesis (Todd's paralysis)

53. Differential diagnosis
 CNS tumour
 Subdural haemorrhage
 Seizure (Todd's palsy)
 Hypoglycaemia
 Hyperglycemia
 Drug overdose (if comatose)
 Meningitis
 Migraine

54. Questions?
Thank you for listening :)

55. Investigations for
Cerebrovascular
Accident (CVA) /
Stroke
By Rosie Vincent
9th Nov 2012

56. How would you know someone is
having a stroke?
• FAST (Face, Arms, Speech, Time)

57. What are the Signs and
Symptoms?
• All strokes tend to be sudden onset, occasionally with
further progression over a few hours. Focal signs relate to
distribution of the affected artery, but collateral supplies
cloud the issue. You can not reliably differentiate between
ischemic and haemorrhagic strokes but some pointers are:
• Ischemic (A): Carotid bruit, AF, past TIA, IHD
• Haemorrhagic (B): Menigism, severe headache, and coma
within hours.

58. Other Symptoms
• Difficulty swallowing
• Excessive drooling
• Choking
• Difficulty walking
• Change in vision (double vision/loss of vision)
• Eyes fail to move in unison
• Difficulty with balance
• Clumsiness
• Loss of coordination
• Symptoms typically occur on one side of the body
• Less common symptoms of a stroke may include:
• Altered smell sense, Headache, Dizziness, Excessive sleepiness,
Excessive salivation, Drooping eyelid, Trismus (can’t open mouth),
Vertigo, Urinary incontinence, Memory loss, Confusion, Delusions,
Coma, Impotence, Generalised weakness, Fatigue

59. Investigation/Examination
• Needs to be prompt!
• Confirm the clinical diagnosis (exclude other causes
e.g. Tumour)
• Distinguish between haemorrhage and ischemic
infarction
• Look for underlying causes for the stoke, therefore we
can reduce risk factors and prevent further strokes
• Identify where the stroke has occurred, what has been
damaged and how it is affecting the patient- So we can
start to plan treatment/management and
rehabilitation.

60. Awareness and consciousness –
Glasgow coma scale/AVPU

61. Cranial Nerve Exam
• Cranial nerves 1 and 2 originate from the cerebrum,
whereas 3-12 originate from the brain stem. Therefore
strokes in these areas may affect the function of these
nerves.
• You know what each one does so think about what
symptoms you might get e.g.
• 1 (Olfactory)= altered smell
• 2(Optic)= loss of vision (total/ partial), Pupil Un-
reactive to light
• 9(Glossopharyngeal)=?

62. Neurological Exams
• Motor and Sensory examination
• If the area of the brain affected contains one of the three
prominent Central nervous system pathways—the
spinothalamic tract, corticospinal tract, and dorsal column
(medial lemniscus), symptoms may include:
• hemiplegia and muscle weakness of the face
• numbness
• reduction in sensory or vibratory sensation
• In most cases the symptoms are usually on just 1 side of
the body, with the defect in the brain on the opposite side
(depends on which part of the brain is affected)
• BE CAREFUL - The symptoms do not always mean there is a
stroke- as these pathways also travel in the spinal cord and
lesions there can produce the same symptoms.

63. Cerebral Cortex
• If the cerebral cortex is involved the CNS pathways can again be
affected, but also can produce the following symptoms:
• Aphasia (inability to speak or understand language from involvement
of Broca's or Wernicke's area)
• Apraxia (altered voluntary movements)
• Visual field defect
• Memory deficits (involvement of temporal lobe)
• Hemineglect (involvement of parietal lobe)
• Disorganized thinking, confusion, hypersexual gestures (with
involvement of frontal lobe)
• Anosognosia (persistent denial of the existence of a, usually stroke-
related, deficit)
• If the ''cerebellum'' is involved, the patient may have the following
symptoms:
• trouble walking
• altered movement coordination
• vertigo and or disequilibrium

64. Stroke Classification
(Bamford/Oxford classification)
• Total Anterior Circulation Infarct (TACI)
• Combination of new higher cerebral dysfunction (eg,dysphasia);
homonymous visual field defect; and ipsilateral motor and/or sensory
deficit of at least two areas of face, arm and leg.
• Partial Anterior Circulation Infarct (PACI)
• Two of the three components of the TACI syndrome with higher
cerebral dysfunction alone, or with a motor/sensory deficit more
restricted than those classified as LACI
• Posterior Circulation Infarct (POCI)
• Ipsilateral cranial nerve palsy with contralateral motor and/or
sensory deficit;bilateral motor and/or sensory deficit; disorder of
conjugate eye movement; cerebellar dysfunction without ipsilateral
long tract deficits; or isolated homonymous visual field defect.
• Lacunar Infarct (LACI)
• Pure motor > 2/3 face, arm, leg Pure sensory > 2/3 face, arm, leg Pure
sensorimotor > 2/3 face, arm, leg Ataxic hemiparesis, No higher
dysphasia or visuospatial or hemianopia or vertebrobasilar problems

65. Investigations - Bloods
• Baselines FBC, U+E Clotting and
ESR
• Random Glucose -Do they have
hypoglycaemia or
hyperglycaemia. Diabetes??
• Lipid Profile –Do they have
hyperlipidaemia
• Hyperhomocysteinaemia?
• Hyperviscosity - Polycythaemia?
• Infection- Vasculitis?
• Prothrombotic States –
Thrombophilla? (Blood clotting
disorders)
• Syphilis?
• Thrombocytopenia?
• Genetic Tests: Check for Fabry’s
disease and CADASIL

66. CT- Computerised Tomography
• CT has the advantage of being available 24 hours a day
• Non-Contrast CT is the gold standard for haemorrhage,
haemorrhage on MR images can be quite confusing.
• On CT 60% of infarcts are seen within 3-6 hours and
virtually all are seen in 24 hours.
• The overall sensitivity of CT to diagnose stroke is 64% and
the specificity is 85%.
• It may be difficult to identify early cerebral infarction
• Posterior fossa and brainstem regions may not be visible
• May not detect small infarcts
especially lacunar infarcts
• Can not differentiate between
old infarcts and old
intracerebral haemorrhages

67. MRI- Magnetic Resonance Imaging
• Not as easily available as takes longer to organise
• Has a specific sequence (stroke sequence) called
Diffusion-weighted imagine (DWI)- this becomes
positive within minutes-hours of stroke onset as a
white ‘light bulb’ which remains for 2-3 weeks
• DWI can detect the haemorrhage as early as CT
• Much better at visualising the posterior fossa
• More sensitive to small infarcts (95%)
• You can differentiate between
old infarcts and haemorrhages
(with MRI + gradient echo)

68. CT vs. MRI
In summary MRI is a lot easier to diagnose due to DWI
changes being so apparent, making the diagnosis
relatively easy for the non-specialist...
BUT CT can differentiate between infarction and
haemorrhage instantly, and is faster to carry out,
therefore it is usually the 1st line approach and is
carried out ASAP after patients admission
CT MRI

69. Investigation for Signs of
Hypertension
• Retinopathy- Ophthalmoscopy/Fundoscopy
• Nephropathy- U+E’s (Urea:Creatinine) Renal
ultrasound, Urinalysis
• Big heart- CXR
• Blood Pressure commonly high in early stroke but
usually do not treat! It may harm the patient and even
a 20% decrease may compromise brain perfusion as
auto regulation is impaired

70. Investigation for Signs of
Cardiac sources of Emboli
• 24 tape ECG – Do they have AF?
• CXR - Enlarged left atrium?
• Echocardiogram (Transoesophageal is more sensitive
than transthoracic) Looking for:
• Mural thrombus due to AF or a hypokinetic segment
of cardiac muscle post-MI
• Valvular lesions which could be due to ineffective
endocarditis or rheumatic heart disease
• Patient foramen ovale (especially in younger patient)

71. Signs of Carotid Artery
Stenosis
• Carotid Doppler Ultrasound
• CT/MRI Angiography

72. Assessing handicap, disability
and independence in daily life
• Two people with the same
impairment (e.g. Paralysed arm)
may have different disabilities
(One can dress and the other
cannot)
• Treatments are usually aimed at
reducing disability and improving
quality of life, not curing disease.
• Usually use Barthel’s Index of
activities of daily living to establish
the patient’s degree of
independence from any help. You
score the patient on the following
aspects of daily living, and total
the scores, gaining a value from 0-
20 (20 = completely able).
• For example: Bowels
0 = incontinent (or needs to be given
enema)
1 = occasional accident (once/week)
2 = continent
• This is also carried out for:
• Bladder
• Grooming
• Toilet use
• Feeding
• Transfer
• Mobility
• Dressing
• Stairs

73. Summary
After carrying out these investigations and examinations on a
patient you should know:
• If they had a stroke
•What type of stroke it was
•Where the stroke occurred
•What caused the stroke
•What the stroke’s effects have been on the patient
Knowing this will now enable you to inform the patient what
has happened to them, and together you will be able to decide
on treatment/management that is best tailored to the patients
needs.

74. The End
Q&A

75. Cases
CVA
Ella Ward-Baker

76. Case 1
• 55 year old woman presents Tuesday morning
feeling faint.
• Notable left-sided hemiparesis and dysarthria.
• Consequently unable to break her fall as she
fell
What other relevant information might we
need?

77. Onset and duration
• Came on within 5 minutes (walking from
home to the bus stop)
• Resolved after 10 minutes
• Followed by another episode that came on
within 5 minutes of arriving at hospital

78. Other necessary information
Prior to episode Mrs X had been getting ready
for work…
• No chance of head trauma
No history of bleeding disorders…
Past medical history of Hypertrophic
cardiomyopathy
• Less likely to be haemorrhagic stroke

79. Other necessary information
What does the medication reveal?
• Bisoprolol 7mg/day – used to treat hypertension
• Hypertension is a risk factor for both ischaemic
and haemorrhagic stroke, exacerbated by
patient’s hypertrophic cardiomyopathy
Family history?
Mother and father both died of MI

80. Investigations
• CT scan
• Labs: U&Es, FBC, Glucose
• ECG
• Carotid Doppler
• Physical examination

82. • CT Scan:
No sign of haemorrhage
No sign of infarction – may not appear for 6-24
hours or up to one week (if at all)
Investigations

83. Left hypertrophic cardiomyopathy…
Don’t be misled into thinking this woman’s symptoms are because of a cardiac
emergency, however this may be another factor leading to her stroke…

84. ECG
• Left hypertrophic cardiomyopathy…
• Patient also known to have paroxysmal AF…
Emboli more likely to form due to impeded
passage of blood through the heart
From there, emboli may travel easily to brain,
causing stroke

85. Other results
• Bloods: Normal
• Carotid Doppler – no sign of stenosis
• Physical examination – no bruits, BP 148/78,
slightly tachycardic, aforementioned
neurological symptoms

86. Management
• Alteplase
Tissue Plasminogen activator
Thrombolytic treatment
• Warfarin
Because of intermittent AF
Inhibits factors… II VII IX X

87. Criteria for Atleplase:
• Present within 3 hours of symptoms (as
infarcted tissue more prone to bleeding)
• CT rules out haemorrhage (would be bright
white bleed on CT)
• Thrombolysis must take place in specific
stroke unit (reason why there is always a bed
kept spare on the ward)

88. Non-Pharmacological interventions
(MDT)
• Physiotherapy – Important to encourage
patient to use affected limbs/relearn use…
- Even once partial use is regained, muscle
wasting from inactivity may be a problem
• Speech and Language Therapy (SALT) –
helping to prevent psychological problems
associated with inability to communicate

89. …
• Occupational Therapist – help the patient by
providing strategies and coping methods to
deal with disability
- Enables patient to begin/continue with daily
tasks/ work/ self-care etc
• Dietician – fair enough to tell a patient to ‘cut
down on salt’, but that doesn’t generally help
in itself…
• Psychological Support

90. Some points about this case
• Highlighted the importance of patient understanding
• On questioning, Mrs X claimed to have no medical
conditions
• On further questioning, hypertension treatment was
mentioned…
• Mrs X then confirmed she had high blood pressure but
that she ‘felt fine’
• She had made no connection between hypertension
and the possible risks - ‘why would that effect my
brain?’
• Patient understanding…

91. • Patient now worried about returning home to
house where she lives alone
• Again, understanding firstly of the risks of
having another stroke, but also what and how
the medication she is on should help her

92. Case 2
• 62 year old man having breakfast with his wife
when he develops a severe headache and
weakness in left arm.
What other relevant information might we
need?

93. Relevant information
• Pain Info
Severe pain localised to head
• Onset
Over 2 hours
• Duration
Ongoing
• Seizure post-admission
• Trauma?
No evidence of trauma

94. Other relevant information
• Past medical history:
-History of Hypertension and hyperlipidaemia
-Hip operation in past 4 weeks
-Has smoked all his life
-No previous stroke
• Medication history
Wafarin 5mg daily

95. Investigations
• Vital signs
• CT
• FBC, Electrolytes
• Echocardiograph – to show cardiac mural
thrombus
• ECG – possible AF
• Plain Chest Radiograph
• Prothrombin Time & Partial Thromboplastin Time

96. • Normal bloods
• Clear Echo, ECG, CXR
• Slightly prolonged PT&PTT
– Related to Warfarin
• BP 160/100
– Not severely hypertensive, so do not treat
hypertension as emergency – lack of evidence as
to whether this is helpful
Results

97. CT

98. Intracerebral Haemorrhage

99. Management
• Anticonvulsants (Seizures most common with ICH
than other strokes)
• Maintain perfusion of the brain
- Keep hydrated (Consider saline)
- Consider intubation if airway patency becomes a
problem
• IV vitamin K & Prothrombin complex
- Reverse anticoagulation treatment
• Send Type & Screen bloods to blood bank
• MDT

100. Thank you