Transcript Localising the lesion *where in the CNS*

LOCALISING THE LESION:
“WHERE IN THE CNS”
Kate Hassan
LEARNING OBJECTIVES
Definition of CNS and PNS
 Definition of UMN and LMN
 Function of each of the cerebral lobes
 The homunculus
 Circle of willis and blood supply to the cerebral
hemispheres
 Motor tracts – lateral corticospinal
 Sensory tracts – lateral spinothalamic and dorsal
columns
 Stroke syndromes
 Clinical case scenarios
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DEFINITIONS
CNS = Brain and spinal cord
 PNS = anything outside brain and spinal cord
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Also include autonomic nervous system and cranial
nerves
MOTOR CONTROL SYSTEMS
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Corticospinal (pyradmial)
Skilled, intricate, strong and organised movements
 Defectiveness  loss of skilled voluntary movement,
spasticity and reflex changes
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Extrapyradimal system
Fast, fluid movements that the corticospinal system has
generated
 Defectiveness  bradykinesia, rigidity, tremor, chorea
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The cerebellum
Co-ordinating smooth and learned movement initiated by
the pyradimal system and in posture and balance control
 Defectiveness  ataxia, past pointing, action tremor and
incoordination
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CORTICOSPINAL (PYRADIMAL) SYSTEM
THE HOMUNCULUS
DEFINITION OF UMN AND LMN
UMN SIGNS VS LMN SIGNS
UMN
LMN
wasting
no
yes
fasciculation
no
yes
tone
increased
decreased
Power
decreased
increased
reflexes
increased
decreased
Plantars
up going
down going
SENSORY PATHWAYS
Peripheral nerves carry sensation from dorsal
roots to the cord
 Posterior columns (dorsal columns)
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Vibration, joint position, light touch and point
discrimination
 Cross in the brainstem passing to the thalamus
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Spinothalamic tracts
Pain and temperature
 Cross within the cord and pass in the spinothalamic
tracts to the thalamus and reticular formation
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Sensory cortex
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Fibres from the thalamus pass to the parietal region
sensory cortex and motor cortex
CEREBRAL LOBES
CORTICAL FUNCTIONS
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Frontal lobe
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Parietal lobe
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Movement, orientation, recognition, perception of stimuli
Occipital lobe
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Reasoning, planning, parts of speech, movement, emotions
and problem solving
Left frontal = broccas area (aphasia)
Visual processing
Temporal lobe
Perception and recognition of auditory stimuli, memory and
speech
 Left temporal = wernicke’s area
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Cerebellum
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Balance and co-ordination
Basal ganglia
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Initiation and inhibition of movement
QUIZ
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Patient has difficulty walking and slurred speech
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Patients wife reported personality change and
difficulty wording what they wanted to say
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Frontal lobe
Patient has difficulty recognising objects and
often gets lost unable to find their way home
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Cerebellum
Parietal and occipital lobe
Patient has difficulty remembering significant
past events and no longer enjoys listening to
music
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Temporal lobe
STROKE SYNDROMES
TACS = total anterior circulation syndrome
 PACS = partial anterior circulation syndrome
 POCS = posterior circulation syndrome
 LACS = lacunar syndrome
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STROKE
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TACS – All three of
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Hemiplegia or hemi sensory loss
Visual field defect
Disturbance of higher function
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PACS – 2 out of 3
LACS – blockage of small branch of big artery
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Dysphasia
Dysphagia
No visual field defect
Pure motor stroke
Pure sensory
Sensory motor
Ataxia
POCS – brain stem, cerebellum, cranial nerves
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Bilateral motor or sensory
Conjugate eye movement disorder
Cerebeller dysfunction
Hemiplegia or cortical blindness
STROKE
Acute occlusion of blood vessel leading to hypoxia
and infarction
 Risk factors
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Investigations
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DM, hypertension, smoking, hypercholesterolemia,
FHx, AF
bloods, CT, MRI, carotid dopplers, Echo, ECG, 24
hour tape
Treatment in ischaemic stroke
Aspirin
 Clopidogrel
 Supportive management
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CEREBELLAR SYNDROME
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Causes
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Vascular lesion
Alcohol
Demyelination
Tumours
Hypothyroidism
Metabolic disorders
Signs “DANISH”
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Dysdiadochokinesis
Ataxia
Nystagmus
Intention tremor
Slurred speech, dysarthria
Hpyotonia, hyporeflexia
MULTIPLE SCLEROSIS
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Areas of demyelination and perivascular
inflammation (white plaques)
Disseminated in time and occurring anywhere within
CNS
Aetiology - ?autoimmune ?vitamin D deficiency
Classification
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Benign
Relapse remitting
Secondary chronic progressive
Primary progressive
Investigations
LP – increased protein, increased immunoglobulin,
oligoclonal bands
 Visual evoked potentials
 MRI
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MULTIPLE SCLEROSIS
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On examination
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Brown-sequard syndrome
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Unsteady gait
Reduced proprioception
Brisk reflexes
Loss of movement on same side as damage
Loss of pain and temp and sensation on opposite side
Management
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Symptoms control (tremors, pain, muscle spasms)
steroids
Beta-inferons
Glatiramer
IV natalizumab
MOTOR NEURONE DISEASE
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Degeneration of upper and lower motor neurones of
unknown cause
5-10% autosomal dominant
Types
Spinal muscular atrophy – limb weakness due to involvement
of spinal cord anterior horn cells
 Primary later sclerosis – spastic limb weakness due to UMN
involvement of the spinal cord
 Progressive bulbar palsy – involvement of bulbar motor
neurones, progressive disease
 Amyotrophic lateral sclerosis – mixture of all the above
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Investigations
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Diagnosed clinically after other causes excluded
EMG confirms fasciculation's and fibrillations
Management – symptom control
Fatal within 3-5 years
MOTOR NEURONE DISEASE
Cardiac and smooth muscle aren’t involved and
ocular muscle very rarely
 Autonomic dysfunction occurs late
 Signs
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Dysarthria, brisk jaw reflex
 Fasciculation/wasting in deltoids, biceps, quadriceps
and in tongue
 Weakness in all4 limbs, brisk reflexes in arms,
absent in legs
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Combination of UMN and LMN
CLINICAL CASE 1
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23, female presents to her GP with a 2 week
history of bilateral leg weakness having started
with pins and needles and numbness in her
hands and feet. She has had a few days of
urinary incontinence which has resolved. 2 years
ago she had an episode of blurred vision and pain
in the right eye which lasted a month and fully
resolved
CASE 1
What is the most likely diagnosis?
 What other signs or symptoms might you see in
this condition?
 What is the pathological basis of this disorder?
 What further investigations would you do?
 How would you manage this patient?
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CLINICAL CASE 2
61 female
 Becoming increasingly weak on her right side
over a one week period. She is unable to walk and
has slurred speech and right side of her face is
drooping
 Past history of breast cancer
 o/e – right facial weakness, grade 4/5 weakness of
the right arm and leg, right homonymous
hemianopia and some difficulty naming objects
and reflexes are brisk on the right side and her
right plantar response is upgoing
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CASE 2
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What is the likely diagnosis?
CASE 2
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CT head shows extensive oedema surrounding
the subtle impression of a ring enhanced lesion in
the left frontal lobe, extending into the left
parietal lobe. There is associated mass effect
displacing the lateral ventricle
CASE 2
What is the likely cause?
 Other features that may be present?
 What management options are available?
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CASE 3
76 male
 Background of AF (on warfarin) has 2 hour
history of severe global right sided weakness. He
is eye-opening to painful stimuli and is moving
his left side spontaneously. When questioned he
seems confused
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CASE 3
What is his GCS?
 What is the diagnosis?
 What investigations would you do?
 What are the important risk factors?
 How wound you manage this patient?
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CASE 4
56 male
 6 month history of progressive weakness of his
right hand. Also had problems with swallowing
and has choked whilst eating on several
occasions
 o/e he has wasting of his upper and lower limbs
and some fasciculation's were noted his right
plantar was up going and his reflexes were
generally brisk
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CASE 4
Diagnosis?
 What investigations would you perform?
 How would you manage this patient?
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THANK YOU FOR LISTENING
Any questions?