Pattern Recognition- Neuroanatomical Localisation Flashcards
What will focal weakness be like?
In distribution of peripheral nerve or spinal root
Hemi-distribution (one side of the body)
Pyramidal distribution
What will non-focal weakness be like?
Generalised
Predominantly proximal or distal
If truly generalized: including bulbar motor function otherwise quadri- or tetraparesis
What is the distribution of UMN weakness?
Corticospinal distribution; hemiparesis, quadriparesis, paraparesis, monoparesis, faciobrachial
What is the distribution of LMN weakness?
Generalized, predominantly proximal, distal or focal
No preferential involvement of corticospinal innervated muscles.
How will sensory loss in UMN appear?
Central patterm
How will sensory loss in LMN appear?
None, glove, stocking, peripheral nerve or root distribution
How will deep tendon reflexes change in UMN weakness?
Increased (unless very acute (flaccid)
How will deep tendon reflexes change in LMN weakness?
Normal or decreased
How will superficial reflexes change in UMN weakness?
Decreased
How will superficial reflexes change in LMN weakness?
Normal
How will pathological reflexes change in UMN weakness?
Increased
How will pathological reflexes change in LMN weakness?
Normal
How will sphincter function change in UMN weakness?
Sometimes impaired
How will sphincter function change in LMN weakness?
Usually normal (unless for example cauda equine lesion)
How will muscle tone change in UMN weakness?
Increased
How will muscle tone change in LMN weakness?
Normal or decreased
How will muscle bulk change in UMN weakness?
Sometimes hypertrophy
How will muscle bulk change in LMN weakness?
Wasting
Will there be other CNS signs in UMN weakness?
Possibly
Will there be other CNS signs in LMN weakness?
No
What is the UMN weakness pattern?
Increased tone
Brisk reflexes
Pyramidal/corticospinal pattern (=weak extensors in arm, weak flexors in legs)
What is the LMN weakness pattern?
Wasting Fasciculation Decreased tone Decreased or absent reflexes Flexor plantars
What is the pattern of weakness in muscle disease?
Wasting (usually proximal)
Decreased tone
Decreased or absent tendon reflexes
What is the pattern of weakness in NMJ dysfunction?
Fatiguable weakness
Normal or decreased tone
Normal tendon reflexes
No sensory symptoms
What is the pattern of weakness in functional weakness
No wasting
Normal tone and reflexes
Erratic power
Non-anatomical loss
When does UMN weakness occur?
Acute stroke syndromes
SOLs
Spinal cord problems
When does LMN weakness occur?
MND
Spinal muscular atrophy
Lead poisoning
Polio
How does PN involvement in LMN weakness usually present?
Symmetrical polyneuropathy with weakness and sensory symptoms
Frequent DM complication, also toxic, metabolic insults, heritable disorders (young onset and skeletal deformities)
Mononeuropathy due to nerve compression (carpal/tarsal tunnel syndrome, ulner/radial neuropathy) or mononeuritis multiplex (asymmetric polyneuropathy) which occurs in context of DM or vasculitis
When does NMJ disorder weakness occur?
Acetylcholine receptor antibody mediated Myasthenia Gravis- ocular or generalised, inhibition of acetylcholinesterase by organophosphate poisoning, or interference with presynaptic calcium channel function in Lambert-Eaton paraneoplastic syndrome
What is the pattern of weakness in muscle disorders?
Often symmetrical
Often proximal
Very wide DDx
What does a stocking pattern of sensory loss imply?
Length dependent neuropathy
What does a sensory level pattern of sensory loss imply?
Spinal cord lesion
What does a haemianaesthesia pattern of sensory loss imply?
Contralateral cerebral lesion, or with no other signs a non-organic disorder
What does dissociated sensory loss with lost spinothalamic but preserved dorsal column suggest?
Hemicord damage
What does the frontal lobe do?
Generates novel strategies and has executive functions
It enables self-criticism and trying again
The prefrontal cortex connects extensively to other association cortices, basal ganglia, limbic system, thalamus and hippocampus
What signs are associated with frontal lobe dysfunction?
Personality dysfunction
Paraparesis
Paratonia
Grasp reflex
Frontal gait dysfunction (magnetic gait)
Cortical hand
Seizures
Incontinence
Visual field defects (anterior visual pathway incl optic chiasms are beneath frontal lobe)
Expressive dysphasia (Broca’s area is in the dominant frontal lobe)
Anosmia (olfactory pathway is beneath frontal lobes)
What is associated with temporal lobe damage?
Memory dysfunction especially episodic memory
Agnosia (visual and sensory modalities in particular)
Language disorders eceptive dysphasia (Wernicke, dominant hemisphere)
Visual field defects (congruous upper homonymous quadrantanopia)
Auditory dysfunction (Heschel’s gyrus, as hearing is represented bilaterally, deafness is not a cerebral feature)
Limbic dysfunction
Temporal lobe epilepsy
What is associated with parietal lobe damage?
Visual field defect (congruous lower homonymous quadrantanopia)
Sensory dysfunction (visual and sensory modalities in particular)
Gerstmann’s syndrome (disease of the dominant angular gyrus, part of the inferior parietal lobe): Dysgraphia, left-right disorientation, finger agnosia, acalculia
Dyspraxia
Inattention (non-dominant angular gyrus)
Denial
What should be considered when diagnosing movement disorder?
Hyper or hypokinetic
What types of hypokinetic disorders exist?
Parkinsonism/akinetic rigid syndrome
What types of hyperkinetic disorders exist?
Tremor Tics Chorea Myoclonus Dystonia
How is Parkinson’s treated?
Symptomatic treatment with Levodopa replacement or dopamine agonist
For selected patients deep brain stimulation (subthalamic nucleus, globus pallidus int)
What is the MOA of levodopa?
Crosses the blood brain barrier while dopamine does not
Levodopa is then converted to dopamine in the brain while peripheral break down is prevented by the addition of ‘inhibitors of aromatic amino acid decarboxylase (carbidopa)
Thus a carbidopa/levodopa formulation is often prescribed in Parkinson’s
Describe dopamine agonists
Cross the blood brain barrier and act directly as D2-type receptors
These agents include pramipexole, ropinirole, and bromocriptine
Describe MAO-B inhibitors (selegiline, rasagiline) effectiveness in Parkinson’s
Can improve symptoms in patients with mild disease (as monotherapy) as well patients already on levodopa
What does amantadine do?
Blocks NMDA receptors and has a mild attenuation of resting tremor and dystonia
May alleviate levodopa induced dyskinesias
59 year old male in good health until 6 months ago. At that time he developed a tremor, he had no other complaints.
On examination, there is a tremor in the right arm at rest and while he walks, he has a sustained tremor in both arms, and to some degree during FNT. He has a poker face and a slow, deliberate gait. Tone is increased in his right arm and leg. Physical examination is otherwise unremarkable. He and his wife deny medications and alcohol.
Parkinson’s
Structural imaging to address DDX
If symptoms cause problems, initiate treatment with dopaminergic treatment
24 year old student is studying for an exam. As she is reading, she notices that her right arm and leg are numb. Dismissing her symptoms, she recalls that she had similar symptoms 6 or 7 months ago. As she stands up to go to the bathroom, she notices that her vision is blurred and her balance is poor. She remembers that she had double vision 2-3 months ago, which subsided after a coup[le of days. She had not seen a doctor for any of these symptoms as she had out them down to stress. She goes to bed and decides to call her GP on the next morning.
MS
Careful neuro assessment and MRI imaging of brain including gadolinium contrast
If no diagnosis confirmed, meets criteria for initiating disease modifying therapy. Acute disabling relapses can be treated with high dose steroids (oral or IV)
What are the LMN signs of MND?
Fasciculations (incl tongue)
Wasting in groups outside a single myotome
What are the UMN signs of MND?
Increased tone Clonus Loss of dexterity Brisk tendon reflexes (or preserved TR in wasted and/or fasciculating muscles) Babinski sign
How are MRI T1/T2 and FLAIR images used in ischaemic stroke?
To identify old lesions and lesions of non-vascular origin
How is DWI (diffusion weight images) used in ischaemic stroke?
To identify new ischaemic lesions (hyperintensities) and a decrease in signal on the apparent diffusion coefficient of water (ADC map)
How are T2* images used in ischaemic stroke?
To identify bleeds and microbleeds
How are time of flight sequences images used in ischaemic stroke?
To identify occlusions of the extra and intracranial arteries
How is PWI (perfusion weight images) used in ischaemic stroke?
To identify brain areas at risk of ischaemia
How are CT brain images used in ischaemic stroke?
Hyperintenisities – bleed, subtle ischemic signs in the acute phase of stroke (may be normal, early signs: loss of limits of lentiform nucleus, poor grey white matter differentiation, loss of insular ribbon)
How will Lacunar syndromes appear?
No visual field defect
No new higher cortical or brainstem dysfunction
Pure motor hemiparesis, or pure sensory deficit of one side of the body, or sensorimotor hemiparesis or ataxic hemiparesis (dysarthric clumsy hand syndrome or ipsilateral ataxia with crural hemiparesis)
At least 2 of the 3 areas (face, arm, leg) should be involved in its entity
How will posterior circulation syndrome appear?
Any one of: Cranial nerve palsy Unilateral or bilateral motor or sensory deficit Disorder of conjugate eye movements Cerebellar dysfunction Homonymous hemianopia Cortical blindness
How will total anterior circulation syndrome appear?
Hemiplegia and homonymous hemianopia contralateral to the lesion, and
Either aphasia or visuospatial disturbances
+/- sensory deficit contralateral to the lesion
How will partial anterior circulation syndrome appear?
One or more of unilateral motor or sensory deficit, aphasia or visuospatial neglect (with or without homonymous hemianopia)
Motor or sensory deficit may be less extensive than in lacunar syndromes
