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 excludedo 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 reflexo Fasciculation/wasting in deltoids, biceps, quadriceps and in tongueo 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