Neuro Flashcards
Symptoms of bulbar palsy
Flaccid, fasciculating tongue, absent/normal jaw jerk, quiet, hoarse or nasal speech, dysphagia and associated drooling
Bulbar palsy is due to…
Degeneration of CN IX, x, xi and Xii of LMN type, nerves with nuclei in the medulla
DD of bulbar palsy
MND, myasthenia gravis, guillakm-barre, syringobulbia (fluid filled cavities in the brain stem, congenital, trauma or tumour), polio, tumour of brainstem (glioma) Lyme disease, genetic (kennedys syndrome), infarction
Findings in pseudo bulbar palsy compared to bp
Exaggerated jaw jerk shows CN V, stiff spastic tongue not wasted, Donald Duck speech, preserved palatal muscles preserved, mood disturbances (eg giggling)
Pseudo bulbar palsy is due to damage of…
Cortical bulbar tract bilateral damage must occur for symptoms
Causes of pseudo bulbar palsy
Stroke, mnd, ms, severe head injur
a cortical lesion of the …… may cause intellectual impairment, personality change, urinary incontinence, monoparesis/hemiparesis. Damage to the …..may also cause brocca’s aphasia
a cortical lesion of the frontal lobe may cause intellectual impairment, personality change, urinary incontinence, monoparesis/hemiparesis. Damage to the left frontal lobe may also cause brocca’s aphasia
a cortical lesion of the frontal lobe may cause ……..Damage to the left frontal lobe may also cause …..
a cortical lesion of the frontal lobe may cause intellectual impairment, personality change, urinary incontinence, monoparesis/hemiparesis. Damage to the left frontal lobe may also cause brocca’s aphasia
Damage to the…… may cause acalculia (inability to do maths problems), alexia (can’t read), agraphia (can’t write), wernike’s aphasia, R-L disorientation, homonymous field defect.
Damage to the L temporo-parietal lobe may cause acalculia (inability to do maths problems), alexia (can’t read), agraphia (can’t write), wernike’s aphasia, R-L disorientation, homonymous field defect.
Damage to the L temporo-parietal lobe may cause ….
Damage to the L temporo-parietal lobe may cause acalculia (inability to do maths problems), alexia (can’t read), agraphia (can’t write), wernike’s aphasia, R-L disorientation, homonymous field defect.
Damage to the …. may cause confused states, failure to recognise faces, homonymous field defect
Damage to the R temporal lobe may cause confused states, failure to recognise faces, homonymous field defect
Damage to the R temporal lobe may cause ….
Damage to the R temporal lobe may cause confused states, failure to recognise faces, homonymous field defect
Damage to ….. may cause contralateral sensory loss/neglect, agraphaesthesia, homonymous field defect
Damage to either parietal lobe may cause contralateral sensory loss/neglect, agraphaesthesia, homonymous field defect
Damage to either parietal lobe may cause …..
Damage to either parietal lobe may cause contralateral sensory loss/neglect, agraphaesthesia, homonymous field defect
Damage to the …. may specifically cause dressing apraxia and failure to recognise faces
Damage to the right parietal lobe may specifically cause dressing apraxia and failure to recognise faces
Damage to the right parietal lobe may specifically cause ….
Damage to the right parietal lobe may specifically cause dressing apraxia and failure to recognise faces
Damage to the L parietal lobe may specifically cause ….
limb apraxia
Damage to the occipital/occipitoparietal lobe may cause ….
visual field defects, visuospacial defects, disturbances of visual recognition
Damage to the ….. may cause visual field defects, visuospacial defects, disturbances of visual recognition
visual field defects, visuospacial defects, disturbances of visual recognition
…….may cause partial seizures, focal motor seizures of contralateral limbs, conjugate deviation of head and eyes away from lesion
Irritative cortical lesions to the frontal lobe may cause partial seizures, focal motor seizures of contralateral limbs, conjugate deviation of head and eyes away from lesion
Irritative cortical lesions to the frontal lobe may cause ….
Irritative cortical lesions to the frontal lobe may cause partial seizures, focal motor seizures of contralateral limbs, conjugate deviation of head and eyes away from lesion
….. may cause formed visual hallucinations, complex paratial seizures, memory disturbances eg deja vu
Irritative cortical lesions to the temporal lobe may cause formed visual hallucinations, complex paratial seizures, memory disturbances eg deja vu
Irritative cortical lesions to the temporal lobe may cause …..
Irritative cortical lesions to the temporal lobe may cause formed visual hallucinations, complex paratial seizures, memory disturbances eg deja vu
Parietal irritative cortical lesions may cause ……
Parietal seizures may cause focal sensory seizures of contralateral limbs
…..may cause focal sensory seizures of contralateral limbs
Parietal irritative cortical lesions
Parieto-occipital irritative lesions may cause
crude visual hallucinations (eg, shapes in one part of visual field)
….. may cause crude visual hallucinations (eg, shapes in one part of visual field)
Parieto-occipital irritative lesions
Occipital irritative lesions may cause
visual disturbances (eg flashes)
may cause visual disturbances (eg flashes)
Occipital irritative lesion
the lateral lobes of the cerebellum control….
co-ordination of movement of ipsilateral limbs
….. maintain axial/midline posture and balance
the vermis/midline structure of the cerebellum maintain axial/midline posture and balance
the vermis/midline structure of the cerebellum maintain axial/midline …..posture and balance
axial/midline posture and balance
what symptoms will occur with a cerebellum lesion?
DASHING
Dysdidokokinesiahw
Ataxia (truncal. Broad ataxic gate)
Slurred speech
Hypotonia and hyporeflexia of limbs
Intention tremor with past pointing and dysmetria (movements inprecise in direction/force and distance) and titubation (rhythmic head movement in yes-yes/no-no movements)
Nystagmus, course, horizontal with fast component towards lesion
what symptoms would occur from a midline/vermis cerebellar lesion?
difficulty standing/sitting unsuppoorted, truncal ataxia (broad ataxic gate), vertigo and vomiting if extending to 4th ventricle
vomitting in ataxia will occur if lesion extends to…
4th ventricle
nystagmus in cerebellar lesions will be
course, horizontal and have fast component towards lesion
what is titubation which occurs due to cerebellar lesions
rhythmic head movements in YES/NO directions
what is dysmetria which occurs due to cerebellar lesions
movements inprecise in direction/force and distance
what clinical syndromes may arise from a basal ganglia pathology
parkinsonism, huntington’s and hemiballismus
In a disorder of the basal ganglia there may be….
BAR CHATD
Bradykinesia (slowness of speech/movement
Akinesia (no movement)
Rigidity of muscles
Involuntary movements including….
Chorea (jerky involuntary movements)
Hemiballismus (violent involuntary movement usually restricted to one arm involving proximal muscles)
Athetosis (Writhing involuntary movements usually of hands, face and tongue)
Tremor
Dystonia (spasms/abnormal muscle control)
Describe Hemiballismus
due to basal ganglia lesion. Hemiballismus (violent involuntary movement usually restricted to one arm involving proximal muscles)
parkinson’s disease is due to
degeneration of the substantia nigra dopaminergic neurones. Pathological hallmark of this is Lewy bodies in this area
Signs of Parkinsons
TRAMP
Tremor, pill rolling, 4-6 hz
Rigidity (lead pipe resistance to passive movement)
Akinesia/bradykinesia
Monotone voice and expressionless face
Postural instability and short, shuffling gate
Damage to the ……would cause a bitemporal hemianopia (loss of both temporal visual fields)
Damage to the optic chiasm would cause a bitemporal hemianopia (loss of both temporal visual fields)
Damage to the optic chiasm would cause a ……
Damage to the optic chiasm would cause a bitemporal hemianopia (loss of both temporal visual fields)
Damage to the optic radiation (parietal/occipital lobe) will cause ……
Damage to the optic radiation (parietal/occipital lobe) will cause contralateral homonymous hemianopia (loss of opposing side of both eye’s visual field or loss of nasal visual field in ipsilateral eye and temporal VF in contralateral eye)
Damage to the …… will cause contralateral homonymous hemianopia (loss of opposing side of both eye’s visual field or loss of nasal visual field in ipsilateral eye and temporal VF in contralateral eye)
Damage to the optic radiation (parietal/occipital lobe) will cause contralateral homonymous hemianopia (loss of opposing side of both eye’s visual field or loss of nasal visual field in ipsilateral eye and temporal VF in contralateral eye)
damage to the …. would cause contralateral superior quadrantanopia (damage to upper half of contralateral temporal VF and ipsilateral nasal VF)
damage to the temporal loop of the optic radiation would cause contralateral superior quadrantanopia (damage to upper half of contralateral temporal VF and ipsilateral nasal VF)
damage to the temporal loop of the optic radiation would cause ….
damage to the temporal loop of the optic radiation would cause contralateral superior quadrantanopia (damage to upper half of contralateral temporal VF and ipsilateral nasal VF)
UMN lesion signs
spastic increase in tone/paralysis, exaggerated tendon reflexes, extensor plantar response, no muscle wasting, loss of fine finger/toe movements, loss of abdominal reflexes, drift of upper limb, normal electrical excitability of muscles
LMN lesion signs
weakness/paralysis, wasting, hypotonia, reflex loss, fasciculations
contractures of muscle and trophic changes in skin and nails long term
definition of TIA
Sudden focal loss, (weak limb, aphasia, loss of vision) lasting less than 24 hours with complete recovery
Amaurossi fugax definition
sudden loss of vision in one eye, often occuring with TIA, often 1st clinical evidence of internal carotid stenosis. Also occurs as benign event in migraine
definition of stroke
sudden focal deficit lasting more than 24 hours/causing death which has no other apparent cause but vascular
what risk factors predispose to a cerbral infarction? by how much?
largely, obesity, diabetes, hypertension, smoking, carotid artery stenosis, moderately inactive lifestyle, alcohol, hypercholesterolaemia, raised haematocrit, AF, sleep apnoea
which risk factors predispose someone to a cerbral haemorrhage
largely, hypertension, obesity, smoking and poosibly AF
Which factors predispose someone to a stroke from a SAH
smoking and hypertension
Describe a SDH
Collection of blood in subdural space following rupture of a vein. Usually follows head injury which can be trivial but can occur spontaneously
Which factors predispose somebody to a chronic SDH? why?
Elderly (veins become brittle and taut by shrinkage), alcoholism, reduced blood clotting
clinical presentation of chronic SDH
fluctuant symptoms occuring within days/weeks/months, headache, drowsiness, confusion, focal deficits (hemiparesis/sensory loss), personality change, epilepsy (occasionally), stupor, coma and coning could follow
how would a CT look in a SDH?
clot plus midline shift, crescent shaped collection of blood over 1 hemisphere which differentiates subdural from extradural
differential dx of SDH could also include
cerebral tumour, dementia, evolving stroke
abnormalities which commonly predispose to SAH
Berry Aneurysm, 70%, arteriovenous malformation, 20% no lesion found in 10%
less common factors predisposing to SAH
Bleeding disorders, endocarditis, acute bacterial meningitis, brain tumours, arteritis (eg SLE), coarctation of aorta, marfan’s, ehler’s danlos, polycystic kidneys, spinal Arteriovenous malformation
signs/symptoms of SAH
- a sudden and severe headache – it has been described as a ‘thunderclap headache’, similar to a sudden hit on the head, resulting in a blinding pain unlike anything ever experienced before, often radiating to back of head
- stiff neck
- feeling and being sick
- loss of consciousness or convulsions (uncontrollable shaking)
- stroke-like symptoms such as slurred speech and weakness on one side of the body
what is the investigation of choice for a SAH. What will the findings be?
CT. will show blood within48 hrs, can estimate load of blood and grade of lesion, CT angiogram can also be done to show anatomy
What test may be performed in suspected SAH if not confirmed by CT? What will be the findings?
Lumbar puncture, will be yellow
what can be the complications of SAH
vascular spasm causing widespread ischaemia and swelling around the brain, blockage of CSF drainage causing hydrocephalus. 30% of patients will die immediately, of survivors 30% will rebleed within a year without intervention
which organisms account for around 70% of bacterial meningitis cases in adults
Neisseria meningitides and Strep pneumoniae
What are the symptoms of autonomic dysfunction
dizziness and fainting upon standing up (orthostatic hypotension)
inability to alter heart rate with exercise (exercise intolerance)
sweating abnormalities, which could alternately be too much sweat or insufficient sweat
digestion difficulties due to slow digestion. Resulting symptoms could include loss of appetite, bloating, diarrhea or constipation, and difficulty swallowing.
urinary problems. These can include difficulty starting urination, incontinence, and incomplete emptying of the bladder
sexual problems. In men, this could be difficulty with ejaculation and/or maintaining an erection. In women, this could be vaginal dryness and/or difficulty with orgasm
vision problems. This could be blurry vision, or the failure of the pupils to react quickly enough to changes in light.
Orthostatic hypotension or orthostatic intolerance (a milder form of orthostatic hypotension) are two of the most common conditions resulting from ANS disorders. Orthostatic intolerance, which results in low blood pressure on standing, causes alarming symptoms. These include lightheadedness, fainting, and heart palpitations.
what are the typical signs of meningitis?
photophobia, vomiting, malaise, fever, rigors, development in minutes to hours, irritable and prefers to lie still, neck stiffnes, positive kernig’s sign, papillodema may develop, meningococcal rash
how should a suspected TIA be managed
aspirin (300 mg daily) started immediately
specialist assessment[6]
and investigation within 24 hours of onset of symptoms
measures for secondary prevention introduced as soon as the diagnosis is confirmed,
including discussion of individual risk factors
When should patients suffering an acute stroke have a brain scan?
1 Brain imaging should be performed immediately[16]
for people with acute stroke
if any of the following apply:
indications for thrombolysis or early anticoagulation treatment
on anticoagulant treatment
a known bleeding tendency
a depressed level of consciousness (Glasgow Coma Score below 13)
unexplained progressive or fluctuating symptoms
papilloedema, neck stiffness or fever
severe headache at onset of stroke symptoms.
1.3.2.2 For all people with acute stroke without indications for immediate brain
imaging, scanning should be performed as soon as possible[17]
.
Investigations for patient with suspected stroke
Serum glucose levels Complete blood count (CBC) Electrolyte values Prothrombin time (PT) Activated partial thromboplastin time (aPTT)
Which screening tools can be used to assess the likelihood of a patient having a stroke?
Community, FAST (Face, Arms, Speech, Time)
Hospital, more complicated such as ROSIER scoring (-ve marks for recent seizures/LOC/Syncope, +ve for face, arms, legs, speech, visual field)
How is muscle power graded in neuro exam
0 nil 1 flicker of movement 2 movement cannot overcome gravity 3 movement cannot overcome any resistance 4 movement is weaker than normal 5 normal
What pattern of weakness is usually seen in an UMN lesion
flexors > extensors in upper limbs
extensors > flexors in lower limbs
Upper motor neurone lesions occur when the damage is above….
the anterior horn
When should lumbar puncture not be performed
GCS <9m suspect raised ICP, bradycardia/hypertension, focal neuro signs, unequal poorly responsive pupils, papilodema, shock, convulsions, coagulation abnormalities, respiratory insufficiency
What signs can be observed for in parkinsons
Inspection
Look for:
- Hypomimia (decreased facial expression)
- Blepharoclonus (fine eyelid tremor)
- Resting tremor (brought out by distraction - such as conversation)
- Tardive dyskinesia (chewing movements of the mouth - drug treatment side effect)
[Return to top]
Face
Look for:
- glabellar tap (keep blinking - normally adjust)
- normal eye movements but abnormal vertical gaze + VOR
(in supranuclear palsy) - speech ? monotonous voice
What additional examinations can be done in a patient with parkinsons
Thank the patient and offer to assist them to get dressed again
Offer to do mmse for Lewis body Offer to take lying and standing blood pressure (autonomic function may be affected in ‘Multi-System Atrophy’ - MSA)
Offer to assess the cerebellar system (this can also be impaired in MSA)
Offer to examine the drugs chart (metoclopramide and neuroleptics can cause Parkinsonian symptoms)
Offer to examine their visual tracking for signs of Progressive Supranuclear Palsy (PSP). Ask the patient to hold their head still and follow your finger with their eyes whilst you move it up in a vertical plane in front of their face. Then, test for the ‘vestibulo-ocular reflex’ by asking the patient to fix their eyes on a point on the far wall, and then move their head up and down by flexing their neck. If a patient is unable to track your finger movements in a vertical plane, but has a retained vestibulo-ocular reflex, then this suggests that there is a supranuclear lesion - in keeping with PSP when it exists with other Parkinsonism signs.
What are the parkinsons plus conditions
Progressive super nuclear palsy, multiple system atrophy (autonomic dysfunction eg postural hypo. Disturbances in urination and sexual function) Cortico basal degen. These will lead to cerebellar and cranial nerve funcs eg swallowing, Lewis body dementia
What is the differential diagnosis of parkinsons
Parkinsons plus; progressive supranuclear palsy, cortico basal degeneration, multiple system atrophy, Lewis body, drug induced (dopamine agonists eg antipsychotics rispiradone), vascular eg stroke basal ganglia or vascular dementia
What are the causes of optic neuritis
The most common cause of ON in regions where MS is relatively common (Caucasian populations and high latitudes).
Ischaemic optic neuropathies Giant cell arteritis (cranial arteritis), anterior and posterior optic neuropathy, diabetic papillopathy.
Corticosteroid-responsive ON Autoimmune diseases, including sarcoidosis, systemic lupus erythematosus,[5] Behçet’s disease, neuromyelitis optica (Devic’s syndrome - affects optic nerves and the spinal cord),[6][7] autoimmune ON, chronic relapsing inflammatory ON.
Other inflammatory causes Post-infection, post-vaccination, neuroretinitis, acute disseminated encephalomyelitis.
