Localising the lesion: “where in the CNS”

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

Definitions

 CNS = Brain and spinal cord

 PNS = anything outside brain and spinal cord

 Also include autonomic nervous system and cranial nerves

Motor control systems

 Corticospinal (pyradmial)

 Skilled, intricate, strong and organised movements

 Defectiveness  loss of skilled voluntary movement, spasticity and reflex changes

 Such as hemiparesis, hemiplegia or paraparesis

 Extrapyradimal system

 Fast, fluid movements that the corticospinal system has generated

 Defectiveness  bradykinesia, rigidity, tremor, chorea

 Such as huntingtons

 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

The motor system

  Pyradimal motor system are the tracts of the motor cortex that reach their targets by
traveling through the "pyramids" of the medulla. The pyramidal pathways the lateral and
anterior corticospinal tracts directly innervate motor neurons of the spinal cord or brainstem
of the anterior horn cells. whereas the extrapyramidal system centers around the
modulation and regulation of the pyradimal tracts via indirect control of anterior horn cells.

 Extrapyramidal tracts modulate motor activity without directly innervating motor neurons.

The corticospinal system

The homunculus
 UMN vs LMN

UMN LMN

Wasting no yes

Fasciculation no yes

Tone increased decreased

Power decreased decreased

Reflexes increased decreased

Plantars up going down going

Sensory pathways
  Peripheral nerves carry sensation from dorsal roots to the cord

 Posterior columns (dorsal columns)

 Vibration, joint position, light touch and point discrimination

 Cross in the brainstem passing to the thalamus

 Spinothalamic tracts

 Pain and temperature

 Cross within the cord and pass in the spinothalamic tracts to the thalamus and
reticular formation

 Sensory cortex

 Fibres from the thalamus pass to the parietal region sensory cortex and motor
cortex

Cortical functions

 Frontal lobe

 Reasoning, planning, parts of speech, movement, emotions and problem solving

 Left frontal = broccas area (aphasia)

 Parietal lobe

 Movement, orientation, recognition, perception of stimuli

  Occipital lobe

 Visual processing

 Temporal lobe

 Perception and recognition of auditory stimuli, memory and speech

 Left temporal = wernicke’s area

 Cerebellum

 Balance and co-ordination

 Basal ganglia

 Initiation and inhibition of movement

 Wernickes area – like broccas area is it the understanding of written and spoken speech

Circle of Willis

Internal carotid artery supplies brain

External carotid artery supplies face

Middle cerebral artery supplies 1/3rd of brain

Vertebral arteries join to form the basillar artery which join at the base of the brain
Stroke

 TACS – All three of

 Hemiplegia or hemi sensory loss

 Visual field defect

 Disturbance of higher function

 Dysphasia

 Dysphagia

 PACS – 2 out of 3

 LACS – blockage of small branch of big artery

 No visual field defect

 Pure motor stroke

 Pure sensory

 Sensory motor

 Ataxia

 POCS – brain stem, cerebellum, cranial nerves

 Bilateral motor or sensory

 Conjugate eye movement disorder

  Cerebeller dysfunction

 Hemiplegia or cortical blindness

 Acute occlusion of blood vessel leading to hypoxia and infarction

 Risk factors

 DM, hypertension, smoking, hypercholesterolemia, FHx, AF

 Investigations

 bloods, CT, MRI, carotid dopplers, Echo, ECG, 24 hour tape

 Treatment in ischaemic stroke

 Aspirin

 Clopidogrel

 Supportive management

 In ischaemic stroke you have in ischaemic penumbra which is the area of the brain which is
damaged during ischaemia in order to reduce the effects from this you need to optimise
conditions – temp, BP, glucose

Cerebellar syndrome

 Causes

 Vascular lesion

 Alcohol

 Demyelination

 Tumours

 Hypothyroidism

 Metabolic disorders

 Signs “DANISH”

 Dysdiadochokinesis

 Ataxia

 Nystagmus

 Intention tremor

 Slurred speech, dysarthria

 Hpyotonia, hyporeflexia

Multiple Sclerosis

 Areas of demyelination and perivascular inflammation (white plaques)

 Disseminated in time and occurring anywhere within CNS

 Aetiology - ?autoimmune ?vitamin D deficiency

 Classification

 Benign -little disease activity for many years, minimal disability

 Relapse remitting - most common, repeated attacks with periods of recovery

 Secondary chronic progressive - continuous progression of symptoms following an

initial relapsing and remitting disease course

 Primary progressive - accumulation of pernament disability over time with

superimposed relapses

 Investigations

 LP – increased protein, increased immunoglobulin, oligoclonal bands

 Visual evoked potentials

 MRI

 On examination

 Unsteady gait

 Reduced proprioception

 Brisk reflexes

 Brown-sequard syndrome

 Loss of movement on same side as damage

 Loss of pain and temp and sensation on opposite side

 spinal cord lesion where there is an incomplete lesion characterized by loss of

motor function loss of vibration sense and fine touch, loss of proprioception  and
signs of weakness on the same side of the spinal injury. This is a result of a lesion
affecting the dorsal column and the corticospinal tract. On the contralateral side of
the lesion, there will be a loss of pain and temperature sensation and crude touch 1
or 2 segments below the level of the lesion

 Management

 Symptoms control (tremors, pain, muscle spasms)

 Steroids - severe relapses to speed up any recovery with will occur naturally. A
severe relapse is usually classed as one that has significantly affected activities of
daily living

 Beta-inferons and Glatiramer - reduce rates of relapses by 30% and is only used in
relapsing and remitting or relapsing progressive disease
  IV natalizumab - is a newer monoclocal antibody treatment used in patients with
very severe active disease that can reduce relapses by 80%, cost, practical
consideration and complications limits its use.

Motor neurone disease

 Degeneration of upper and lower motor neurones of unknown cause

 5-10% autosomal dominant
 Types
o Spinal muscular atrophy – limb weakness due to involvement of spinal cord anterior
horn cells
o Primary later sclerosis – spastic limb weakness due to UMN involvement of the
spinal cord
o Progressive bulbar palsy – involvement of bulbar motor neurones, progressive
disease
o Amyotrophic lateral sclerosis – mixture of all the above
 Investigations
o Diagnosed clinically after other causes excluded
o EMG confirms fasciculation's and fibrillations
 Management – symptom control
 Fatal within 3-5 years
 Cardiac and smooth muscle aren’t involved and ocular muscle very rarely
 Autonomic dysfunction occurs late
 Signs
o Dysarthria, brisk jaw reflex
o Fasciculation/wasting in deltoids, biceps, quadriceps and in tongue
o Weakness in all4 limbs, brisk reflexes in arms, absent in legs
 Combination of UMN and LMN

Clinical case 1

 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

 Diagnosis – MS

 Visual – optic neuritis, diplopia, nystagmus, internuclear opthalmoplegia, dysarthria,

dysphagia, weakness, muscle spasms, ataxia, pain, paraesthesis, fatigue, cognitive
impairment, depression, unstable mood

 Uhthoff’s phenomenum – the worsening of neurological symptoms after periods of exercise

and increased body heat

 Lhermittes sign – an electrical sensation that spreads from the back into the limbs on neck
flexion and or extension

 Bowel problems – incontinence, diarrhoea, constipation

 Urinary – incontinence, frequency, urinary retention

 Plaques of demyelination within the CNS caused by an inflammatory process. Different areas
of the CNS are involved over time
  LP – cell count, protein, glucose and oligoclonal bands. WCC less than 50/mm3

 MRI

 Visual evoked potentions – show delayed conduction between the retina and the occipital
cortex

 There is no curative treatment

 Multidisciplinary team

 Symptomatic – spasticity, pain, fatigue, depression, continence

 Steroids, beta interferon, glatiramer, natalizumab

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

 diagnosis = Cerebral maetastases from carcinoma of the breast

 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

 Features of raised intracranial pressure it is likely the oedema around the tumour has
increased or bleedin has occurred within the tumour

 Features of raised ICP – visual loss, seizures and focal neurological deficit such as third and
6th cranial nerve palsies

 Multidisciplary team, neurosurgery, corticosteroids, radiotherapy, chemotherapy

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
 12/15 E2, V4, M6
 Left hemisphere primary intracerebral haemorrhage causing right sided hemiparesis
 Bloods tests, CXR, head CT
 head CT should have been performed within 24 hours or immediately in patients
presenting with acute stroke if any of the following apply to them. – on anticoagulation
treatment, known bleeding tendancy, decreased consciousness, papliodemea, neckstiffness
or fever, severe headache with sudden onset,
 Ultrasound doppler, cerebral angiography, echocardiography
  Risk factors – hypertension, smoking, DM, FH, increasing age, previous strokes, vascular
disease, hyperlipidaemia, hypercoagulable state, alcohol abuse, malignancy
 In ishcamic stroke – thrombolysis three hours from obsets are elegible
 Aspirin, lipid lowering drugs, anticoagulation if patient has AF or other source of embolus
 Haemorrhaging stroke – supprotive care. neurosurgery

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

 Motor neurone disease

 MRI – to exclude local brainstem pathology

 EMG – acute denervation of the lower motor neurones

 Cases were the diagnosis isn’t clear – LP to exclude MS, muscle biopsy to exclude muscle
disease. Blood tests for other conditions