Week 1 Neurological Symptoms and Pathologies Flashcards
Which of the following are lower and upper motor neurons
Subcortical tracts
Internal capsule
Peripheral nerve
Spinal cord
Muscle
Neuromuscular junction
Cortex
Brainstem (decussation in pyramids)
Anterior horns
Ventral roots
Plexi
What is the function of the internal capsule?
To transport motor information from the cortex to the brainstem and sensory information formt he brainstem to the cortex
What are basal ganglia?
The are subcortical nuclei that act as a check on motor signals
What neurons are affected in pyramidal weakness?
Upper motor neurons
What is the presentation of pyramidal weakness?
Distal muscles weaker than proximal (slow finger/foot taps)
In upper limbs, extensors (e.g. triceps) are weaker than flexors (e.g. biceps)
In lower limbs, the opposite is true; flexors are weaker than extensors
Hint - think of strength as a pyramid with the base proximal and top distal. Also to build a pyramid you need to pick up a block with your biceps and walk it up using your quads.
What do the suffixes paresis and plegia mean?
Mild-moderate weakness if often given the suffix -paresis
More severe weakness is given the suffix –plegia
What would weakness with this distribution be called?
Monoparesis/-plegia: single limb (can be arm or leg)
What would weakness with this distribution be called?
Paraparesis/-plegia: both legs
What would weakness with this distribution be called?
Tetraparesis/-plegia: all four limbs (quadriparesis is another term)
What would weakness with this distribution be called?
Hemiparesis/-plegia: weakness affecting arm and leg on one side
60 year old female
Awoke with weakness in right hand
On examination
- weakness affecting finger and thumb movements in multiple directions (not conforming to a nerve territory)
mild wrist weakness
Sensation normal
What is going on here?
Diagnosis: ischaemic stroke affecting motor hand region (‘hand knob area’)
If there is local motor weakness but sensory is unaffected then you can assume it isn’t a problem with the local nerve. Chord lesion would effect lower limb.
By exclusion we are left with a small localised motor cortex lesion/ infarct
65 year old female
Abrupt onset difficulty walking
Reduced power in left ankle movements including dorsiflexion, plantarflexion
Ankle reflexes preserved
Left plantar reflex upgoing
Sensation normal
Diagnosis: small haemorrhage in motor region supplying distal lower limb
If there is local motor weakness but sensory is unaffected then you can assume it isn’t a problem with the local nerve. Upgoing reflex hints at lesion above the segment of the reflex arc (part of spinal chord responsible for reflex)
By exclusion we are left with a small localised motor cortex lesion/ infarct
What parts of the body and in what ways would be affect by a Corona radiata or capsule lesion/ bleed?
Tracts travel closely together therefore lesions here affect broad anatomical territory with both motor and sensory effects e.g. hemiparesis +/- hemisensory disturbance
What is important to remeber with the side that effects of a brainstem lesion occur?
The lesion is above the decussation of the pyramids.
Hence, crossed signs arise:
- ipsilateral cranial nerve locations
- contralateral signs in limbs
What does a hyperactive stretch reflexe indicate?
Hyperactive stretch reflexes are seen when there is interruption of the cortical supply to the lower motor neuron, an “upper motor neuron lesion.” The interruption can be anywhere above the segment of the reflex arc aka anywhere above the part of spinal chord responsible for the reflex?
How does a cervical chord lesion present?
Lesion affecting bilateral cord will produce weakness in all four limbs (tetra-)*
Once established, spasticity and brisk reflexes will be present, with upgoing plantars
Other markers of a cord lesion include sensory loss (with a ‘level’) and disturbance to bowel and bladder (sphincter) function
40 year old man
2 weeks progressive walking difficulties
Weak and numb hands with clawing fingers
Difficulty emptying bladder
Tetraparesis, spasticity in all 4 limbs, hyperreflexic
Diagnosis: prolapsed intervertebral disc causing cervical myelopathy
Important part: affecting the cervical chord
70 year old man
12 months progressive walking difficulties, accelerated decline last 3 weeks
Difficulty weight bearing; using crutches
Difficulty emptying bladder
Exam: bilateral pyramidal weakness in legs with spastic tone, brisk reflexes, upgoing plantars, sensory disturbance (all modalities)
Diagnosis: multilevel degenerative disc disease with prolapsed disc causing compressive myelopathy at T11
Important part: affecting the thoracic chord
How does a thoracic chrod lesion present?
If this produces weakness it will affect lower limbs, and not upper limbs
Spastic tone, pyramidal weakness, brisk reflexes, upgoing plantars
Will also see
- sensory disturbance (with specific level demonstrating site of lesion in the spine)
- sphincter disturbance
How does cauda equina syndrome present?
Lesions here can cause bilateral paralysis, sensory loss, LMN signs (e.g. areflexia) and loss of bladder/bowel function
Given where the nerves leave the spinal chord compared to where they leave the vertebre it could present similarly to a lower thoracic spinal chord lesion however the key difference that gives it away as LMN will be diminished reflexes
50 year old woman
Acute back pain with radiation down legs (radicular type)
Unable to weight bear
New urinary incontinence, faecal soiling
Exam:
Weakness of hip extensors, loss of ankle reflexes, loss of sensation in L5 and S1 territories, reduced anal tone on rectal exam
Likely diagnoses?
Large central disc herniation at L4/5 space causing cauda equina syndrome
How does a root lesion present?
What is the word for root compression?
Spaces where nerves exit the spinal canal are vulnerable to compression (radiculopathy)
Common cause is prolapsed intervertebral disc
Other causes can include facet joint hypertrophy, spondylolisthesis
- can also include inflammation (radiculitis)
Symptoms include pain which radiates down the nerve (radicular pain), dermatomal sensory loss +/- weakness in the site (LMN signs on exam; areflexia, wasting)
Examination may elicit characteristic pain via provocative manouevers (e.g. straight leg raise), loss of reflexes in affected territory
Similar presentation to cauda equina however will be more localised
How would a plexus lesions present?
Plexus lesions would typically be unilateral and have LMN lesions characteristics e.g. weakness, sensory loss and reduced reflexes.
However plexus lesions produce a pattern of weakness not conforming to an individual root territory, nor peripheral nerve
What is this called and what is it an example of?
It is called a Pancoast tumour
Apical lung tumour can invade lower segments of brachial plexus hence an example of a plexus lesion
Patients may present with weakness and wasting of intrinsic hand muscles
- May be first sign of cancer
Hint: Panko breadcrumbs
How does a periferal nerve lesion present? What is a another word for it?
Lesion affecting individual nerve = mononeuropathy
Signs will reflect loss of function in the region supplied by the specific nerve
Usually sensory +/- motor features
Some nerves are sensory- or motor-only however
Nerves can become damaged by a variety of processes, including compression, inflammation, tumours
How does polyneuropahpy present?
Can you give an example?
Multiple nerves affected in multiple limbs (+/- cranial nerves)
Various patterns exist, but in general: longest nerves damaged first
Length-dependent pattern arises: ‘glove and stocking’ sensory loss, distal weakness
Reflexes diminished / absent
Chronically (weeks-months) will see wasting, sometimes fasciculations
An example would be Guillian-Barr syndrome
What happens with a neuromuscular junction problem?
It is caused by the NMJ being ineffecient, either acetylcholine supplies exaust quickly or the few receptors saturate quickly.
This results in fatiguable weakness
How does an NMJ problem present? Which muscles does it effect?
Fatiguable weakness
Sensation normal
Effects the following areas:
- Proximal muscles (hip, shoulder, and neck)
- Ocular muscles
- Bulbar muscles (dysarthria, disphagia, loss of airway tone)
What is this?
50 year old woman
Difficulty keeping eyes open
Intermittent double vision
Slurred speech
Difficulty chewing food and swallowing
Some difficulty standing from a chair
-> Symptoms worse at end of the day (diurnal pattern)
Examination: ptosis, worsening on sustained upgaze; proximal muscle weakness worse on sustained exertion (fatiguability)
Myasthenia Gravis
This is a autoimmune dissorder where antibodies are produced for the acetylcholine receptors
Remaining receptors quickly saturate resulting in fatiguable weakness
Treatment of Myasthenia Gravis?
- Pyridostigmine (acetylcholinesterase)
- Immunosuppression (steroids, azathioprine, IVIg)
- Supportive measures (e.g. feeding tubes, rehabilitation)
- In some cases, surgery: association with thymoma (paraneoplastic disorder)
- Avoid certain drugs which may worsen the disorder (e.g. gentamicin)
Presentation of Myopathy
Many diseases exist affecting muscles
As with neuropathy, many different patterns exist
In general however: pattern is of proximal weakness
-> fatiguability is not seen (in contrast to NMJ)
-> reflexes are generally preserved
-> sensation is normal
Other features include characteristic regions of atrophy (or hypertrophy), contractures, pain, dysmorphic features
What is this?
66 year old man
Last 2 months: progressive difficulty in walking, now unable to climb stairs, stand from sitting
Also difficulty raising arms to comb hair
Some discomfort in muscles
Exam:
-difficulty standing from sitting: leans on hands
- non-fatiguable weakness in hip and shoulder groups; normal reflexes
Investigations:
-elevated creatine kinase (CK)
- Muscle biopsy: inflammation and invading lymphoid cells
Polymyositis
What is polymyositis and what is the treatment?
Autoimmune disorder causing muscle inflammation
May sometimes be associated with underlying cancer (paraneoplastic phenomenon)
Treatment:
* Immunosuppression: steroids, azathioprine/methotrexate, IVIg
* Supportive measures: physiotherapy, OT, SLT
* Screen for underlying cancer - and treat if present
65 year old man
Gradually progressive symptoms
Began with tripping easily
Last 4 months: slurred speech
Now difficulty using left hand for fine motor tasks (e.g. buttons, laces)
Exam:
* dysarthric speech
* wasting in 1st dorsal interosseous
Weakness in finger movements
* Increased tone in ankle with clonus
Brisk right biceps jerk, absent right knee, brisk right ankle
* Upgoing left plantar
* Sensation normal
ALS
Mix of UMN, LMN and bulbar features affecting multiple regions (leg, arms, bulbar)
No sensory features
Gradual, insidious progression over months
-> Characteristic of motor neuron disease
-> most common form (amyotrophic lateral sclerosis)
Degeneration in descending corticospinal pathways, anterior horns and peripheral motor nerves
Incurable and rapidly fatal condition
treatment is supportive
What does ALS stand for?
amyotrophic lateral sclerosis
a - without
myo - muscle
trophic - nourishment
lateral sclerosis - effects the lateral areas of the spinal chord
Can you fill in this table of presentations of different root lesions?
What arteries supply the spinal chrod and what is the significance of this?
Anterior spinal artery (ASA): The primary blood supply to the anterior two-thirds of the spinal cord. The ASA is formed by the vertebral arteries, which originate from the subclavian artery.
Posterior spinal arteries (PSAs): Supply the posterior third of the spinal cord.
This means infarction of one of these areas can occur
What is the consequences of anterior spinal infarction?
Bilateral weakness - knocked out corticospinal tract
Loss of pain/temperature below the level of the infarct - knocks out spinothalamic tracts
Spared touch, proprioception, vibration
Sphincter disturbance
What do the fasciculi do?
What are the consequences of a posterior spinal infarction?
Gracile fasciculus
Carries sensory information from the lower half of the body, including the lower limbs, and enters the spinal cord at the lumbar level.
Cuneate fasciculus
Carries sensory information from the upper half of the body, including the upper limbs, trunk, and neck, and enters the spinal cord at the cervical level.
The gracile and cuneate fasciculi are part of the posterior columns, which are made up of the central processes of primary sensory fibers. These fibers transmit information about touch, vibration, and proprioception from the same side of the body
Selective loss of touch, proprioception and vibration
Clinically, sensory ataxia
Falls
Typically worse balance in the dark (and Romberg’s positive)
Unilateral lesions common in MS
Bilateral: tabes dorsalis (Syphilis), B12 deficiency, Friedreich’s ataxia, compression (e.g. tumour)
What is a common bacteria that can cause Guillain-Barre syndrome?
Campylobacter jejuni
Associated with poultry.
Remember by: Guillain-Barre is a camp drag queen barred from the club so no affects the outside only (periferal de-myelination)
What’s going on here?
A patient complains of difficulty walking – his right leg has become weak
He has also noticed something strange
- his right leg feels numb
- yet when having a bath, he couldn’t feel the water temperature with his left (non-weak) leg
Examination:
- right leg: weakness and loss of fine touch, vibration, proprioception
- left leg: motor function intact. Loss of pinprick and temperature sensation
Hemichord lesion
Motor control travels down the spinal chord on the same side it innervates
Spinothalamic tract travels up the spinal chord on the contralateral side, pain and temperature
Posterior collumn (The gracile and cuneate fasciculi) travels up on the same side, carries fine touch, vibration and proprioception.
Sensory features of a brainstem lesion
Features depend on location
Classic findings = crossed sensory loss
- ipsilateral facial numbness
- contralateral limb & body numbness
Additional features reflect involvement of other tracts and nuclei
- gaze palsy
- pyramidal weakness
- impaired swallow
What are the signs of a cortico sensory deficit e.g. lesion of the sensory cortex?
May lose all modalities in a given region (think homunculous)
May see additional cortical signs (e.g. visual or sensory inattention)
Higher cortical sensations (some sensory processing):
Two-point discrimination
Stereognosis (ability to identify an object’s shape and form by feeling it)
Graphaesthesia (ability to recognize writing or symbols on the skin by touch)
Fill in this table
How do lesions in the midline of the cerebellum differ from lesions in on of the hemispheres?
Midline: manifests as imbalance
Hemisphere: manifests as incoordination
What is this?
Patient presents with sudden onset headache, nausea, unsteady gait and right sided clumsiness
Right sided cerebellar hemorrhage
What is this?
Patient presents with chronic onset cerebellar syndrome
Left sided cerebellar tumour
What is sustained ankle clonus a sign of?
Upper motor neuron lesion.
Sustained ankle clonus is a rhythmic contraction of the ankle muscles that occurs after a sudden stretch, and is considered abnormal if it lasts for five beats or more. It’s a sign of hypertonia, which is caused by a lesion in an upper motor neuron.
Where is the decussation of pyramids?
At the base of medulla oblongata as it transitions tot he spinal chord
What is the only cranial nerve that decussates?
Trochlea nerve (cranial nerve IV)
