Case 3
Hx & Examination
• PC: sudden speech difficulty & right sided
weakness
• Alert & attentive.
• PMH hypertension (BP 172/86), ex smoker and
heavy Eth drinker
• Comprehends simple commands
• speech difficulty (fluency, naming, repetition)
• Right lower facial droop
• weakness of the right arm and leg
What is the likely diagnosis and areas
of the brain affected?
•Left MCA stroke (embolus, thrombus,
haemorrhage) is the probability diagnosis
BROCA'S AREA
WERNICKE'S AREA
MOTOR CORTEX
SENSORY CORTEX
Expressive speech area.
Integration with other language areas.
Receptive speech area.
Integration with other language areas.
Movement of right head and neck,
movement of right arm and possibly right leg
Sensation from right head and neck,
sensation from right arm.
Stroke Mimics
• A study of more than 400 patients initially diagnosed as stroke, 19%
were found to have mimics:
• unrecognized seizures with postictal deficits (17% of mimics). Most
of these patients had postictal confusion or stupor but transient
focal neurological signs were observed in about half of the patients
including hemiparesis (Todd’s paralysis), monoparesis,
abnormalities of extraocular movements, or hemisensory deficits.
• systemic infections (17%), delerium
• hemiplegic migraine: unilateral hemiparesis outlasts the headache.
• brain tumor (15%) - a review of patients with brain tumors
presenting to an ED showed that 6% of patients had symptoms that
were of less than one day’s duration; it was thought that these
patients with brief symptom duration might reflect a subpopulation who suffer acute deterioration from hemorrhage into
the tumor or who develop obstructive hydrocephalus.
• toxic-metabolic disturbances (13%) – hypo natremia/glycemia
• Conversion Disorder: psychiatric, loss of body functions
•
Libman RB, Wirkowski E, Alvir J, Rao TH. Conditions that mimic stroke in the emergency department. Implications for acute stroke trials. Arch Neurol. 1995;52:1119-1122
What is the best next diagnostic step?
What other investigations are warranted?
• Next best diagnostic step
–
–
–
–
–
–
Exclude head trauma (inspect, feel)
ECG to identify arrhythmias (esp. AF) & CHF
CXR
CT (CT angiography)
MRI (Diffusion Weighted shows infarction within minutes)
MRA (magnetic resonance angiogram) to determine if cause is
vascular in origin
• Other investigations
–
–
–
–
FBC, platelets, PTT, INR
U&E’s
Glucose
urinalysis
Q3 What is the best next step in
management?
•
•
•
•
•
•
IV TPA if thromboembolic stroke < 3hrs
Tight glycaemic control with insulin
Control BP
Control arrhythmia
Maintain hydration and renal function
Stockings or pneumatic boots plus heparin to
prevent pulmonary embolism
• Plan and begin rehab (speech, physio, diet)
Define Ischaemic stroke, Transient ischaemic attack & Haemorrhagic stroke
(Intracerebral haemorrhage). Can these be distinguished on clinical grounds?
• A stroke has 4 elements. They are
–
–
–
–
Abrupt
Focal
Rapidly progressing
Irreversible neuronal damage
• A stroke is caused by
– Embolism: deficits appear instantaneously (AF, HF, IE, PFO)
– Thrombus: deficits evolve minutes to days
– Haemorrhage: Intracerebral & sub-arachnoid: deficits are
static or progress over hrs
• A TIA is an abrupt, focal transient loss (< 1-2 hrs –
Murtagh says < 24 hours but “wtf”) of brain function
which doesn’t result in neuronal necrosis.
• They cannot be distinguished on clinical grounds
Review and present the vascular supply of the brain. How would lesions
in the anterior circulation and posterior circulation present?
ACA
MOTOR CORTEX
(Lower Limb)
SENSORY CORTEX
(Lower Limb)
SUPPLEMENTAL MOTOR AREA
(Dominant Hemisphere)
PREFRONTAL CORTEX
Controls movement of the contralateral lower limb.
Receives sensory input from the contralateral lower limb
Functions with Broca’s area in the initiation of speech.
Functions in volition, motivation, and planning and organizing
of complex behaviour.
•Left ACA: Right leg upper-motor neuron weakness due to damage to motor cortex and right leg
cortical sensory loss due to damage to sensory cortex. Grasp reflex, frontal lobe behavioural
abnormalities, and transcortical aphasia can also be seen if the prefrontal cortex and supplemental
motor areas are involved.
•Right ACA: Left leg upper-motor neuron weakness due to damage to motor cortex and left leg
cortical type sensory loss due to damage to sensory cortex. Grasp reflex, frontal lobe behavioural
abnormalities and left hemineglect can also be seen if the prefrontal cortex and non-dominant
association cortex are involved
PCA
Superficial Branch
Occipital Lobe
Corpus Callosum
Primary and secondary visual areas. Functions in the
sensation and interpretation of visual input..
Primary and secondary visual areas. Functions in
the sensation and interpretation of visual input.
Inferior Branch
Thalamus
Relay centre for descending and ascending information
Internal Capsule
Descending fibres of the lateral and ventral corticospinal tracts
•Left PCA: Right homonymous hemianopia due to damage to left visual cortex in the occipital lobe. Extension to
the splenium of the corpus callosum therefore interfering with communication between the two visual association
areas can cause alexia without agraphia. Larger infarcts involving the internal capsule and thalamus may cause
right hemisensory loss and right hemiparesis due to disruption of the ascending and descending information
passing through these structures.
•Right PCA: Left homonymous hemianopia due to damage to right visual cortex in the occipital lobe. Larger infarcts
involving the internal capsule and thalamus may cause left hemisensory loss and left hemiparesis due to disruption
of the ascending and descending information passing through these structures.
Carotid & Vertebrobasilar