Neuro Flashcards
what are the different types of sensory neurons and what do they carry
Alpha- heavily myelinated, proprioception
Beta- less myelinated, crude touch pressure vibration
Delta- least myelinated, cold temperature, sharp pain
C fibres, unmyelinated- hot tempreture dull pain
what are the different types of nerve damage
demylination- post diptheria neuropathy, GB sybdrome
axonal damage- denegerative, toxic neuropathy (commonest type
compression- Pressure- entrapmentt
Infarction- DM neuropathy
Inflammatory and granulomas- leprosy, granulomas
what is mononeuropathy and its causes
Neuropathy of 1 singular nerve, causes by trauma or entrapment
types of mono neuropathys
Carpal tunnel syndrome bells palsy common peroneal nerve palsy sciatica ulner nerve palsy radial nerve palsy lateral cutaneous nerve of thigh- meralgia parasthesia
investigation and diagnosing mononeuropathys and mononeuropathy complex
nerve conduction studies and history
what is mono neuropathy complex and its cause
neuropathy of a few specific nerves WARDSPLC wengers aids rheumatoid diabetes M Sarcoidosis Leprosy Carcinoma
what is polyneuropathy and its types of presentation
Disorder of peripheral nerves, can be acute or chronic, sensory or motor. commonest is sensory motor
sensory neuropathy presentation
parasthesia,
ataxia - test if ataxia is sensory or centeral, close eyes.
sensory loss
motor neuropathy presentation
Weakness, paresis plegia, paralysis fasiculations, twictching. cramps atrophy
Axonal Polyneuropathy, commonest type and its presentation
symmetrical sensory motor PN
starts ditsally as just sensory and becomes more proximal and more motor
causes of axonal PN
DM, Renal failure, hyopthyroidism malignancy or polycythemia rubra vera Inflammatory, GB syndrome sarcoidosis Vit B12 deficiency Drugs, alcohol induced, metronidazole inherited, charcot mary tooth vasculitis- ANA and ANCA
commonest cause of neuropathy
Diabetic Neuropathy
then Chronic idiopathic axonal neuropathy- probablu inflamatory but unkown
commonest cause of demyelination
Chronic inflammatory immune mediated demyelination- autoimmune- (type of GBS)
then genetic causes like charcot mary tooth syndrome
what is Guillain barre syndrome
acute inflammatory demyelinating neuropathy, can be axonal- only affects peripheral nerves
causes and onset of Guillain barre syndrome
onset after infection, Campylobacter jejuni or cytomegalovirus, actual cause unknown could be vaccines
clinical features of Guillain barre syndrome
usually starts 1-3 weeks post infection. start with parastheis and weakness deveops proximally as time goes on and gets worst over 6 weeks then spontanously improves
affects proximal muscles body like trunk more
can deveopl respiratory muscle wekaness or autonomic signs like retention, bowel and bladder plus erectile dysfunction
diagnoses of Guillain barre syndrome
clinical based on history, can do nerve condction studies.
CSF protien elevated
management of Guillain barre syndrome
IV immunoglobulins improve prognosis
monitor for resp complications may need ventilation
General management for neuropathies
for vasculities or Guillain barre syndrome
Pain- amytriptyline or Gabapentin
balance- physiotherapy and occupational therapist, walking aid, retraining, foot care in neuropathies
GBS- IV Immunoglobulins
Vasculitis- steroids
commonest cause of brain tumour
Secondary tumour that has metastasised from elsewhere usually lung or breast
Types of brain tumour
primary- Gliomas, commonest primary tumour other types, meningioma schwannoma, acoustic neuroma craniophangyoma- in pituitary Secondary
How does a brain tumour present
focal or non focal neurological defects- weakness, dysathia
Generalised or localised seizures
raised ICP will cause ICP headache and papilloedma
feautures of raised ICP hedache
headache, worst at night and in mornings, worst when lie down or cough or exercise.
relieved by vomiting,
assosiated with papilloedma
Dull pain behind eyes
Investigations for Brain tumour
CT or MRI, any new onset seizure = CT Scan
biopsy once confirmed its a tumour to see what kind of tumour it is and treatment options
How are Gliomas Classified
WHO classification of primary Gliomas 1 begin 2 slow growing 3 high grade 4 commonest type- 12 month survivability
causes of primary brain tumours
usually no known cause
associated with ionising radiation at a young age
family history
immunosuppresssion
Treatment of brain tumour
Dexamethasone to reduces brain swelling and oedema
diuretics
Tumour resection or removal (awake craniotomy)
followed by radiotherapy and chemotherapy
what is motor neuron disease and what neurons does it affect or not affect
chronic degenerative disease affecting Upper and lower MNs. does not affect eyes.
does not affect sensory or sphincters
what is the prevalence likely age group and prognosis of MND
Prevalence 6 in 100,000
average onset 60
prognosis 2-4 years
types of MND
Amylotrophic lateral sclerosis- commonest
progressive bulbar palsy
progressive muscular atrophy
primary lateral sclerosis
Presentation of MND
Has both UMN and LMN lesions, no effect on eyes. fasiculations. spasticity. increased tone but weakness.
hyperreflexia
CXR shows raised diaghram bilaterally
Diagnosis of MND
clinical diagnoses
neurophysiology studies- confirms deinnervation
neruoimaging to exclude other causes
Managment of MND
MDT, Physio OT Dietican and social care
avoid chokcing due to dysphagia by belnding food or NG tube
monitor may need Ventilation due to diaphram and resp muscle paralysis
pain- analgesic ladder
drooling- propantheline
antiglutamatergic drugs- Riluzole ( drug that improves prognosis for ALS)
What is mysthenia gravis
autoimmune condition againts acetylecholen receptors AChR antibodies.
neuromuscular junction condition
mysthenia gravis signs and symproms
Increasing muscle fatigue, muscle weakness
fasiculations . gets worst as disease progresses
tender reflexes dissapear over time
sensory not affected.
ptosis, diplopia Extraoccular palsy
mysenthic gnarl
myasthenia gravis where do the symptoms start and where does it progress to
start at eyes, then face, neck trunk, limbs
assosiations of myasthenia gravis
women under 50 with other autoimmune disease
men over 50 withother autoimmune disease, rhematoid SLE and thymus hyperplasia in both
Investigations of Myasthenia gravis
Serology- Anti AChR antibodies
neurophysiology, muscle stimulation gets less after repeated stimulation
CT of thymus.
applying ice pack to closed eyelid for 2 mins= ptosis improves temporarly
Treatments of Myasthenia Gravis
1st and second line pharmacological
Anti acetylcholinesterase - pyridostigmine
2nd line is immune suppression- predniselone
treatment of myasthenia gravis
surgical
Thymectomy,
complications of myasthenia gravis,
myasthenic crisis- respiratory problems, dysphagia
what are the different kinds of headache
Primary - tension, cluster, migraine
secondary - meningitis SAH, GCA, ICP headache, medication overuse headache
Other/cranial neuropathy - trigeminal neuralgia
what are the different kinds of migraines
with auras- classic
without aura - common
classical migraine with auras features
2 attacks in a year.
has at least 1 aura: fully reversible visual or speech distubances
has 2 of: 1 Homonymus visual symptoms/unilateral sensory symptoms. 2 symptoms develop gradually, over 5 minutes. 3 each symptom lasts 5 to 60 minutes
headache usually unilateral throbbing following the auras. can be other character
Not attributable to other causes
common migraine without auras features
5 attacks in a year
onset of pain lasting 4-72 hours
has one of (photo and phonophobia) or (nausea and or vomiting)
has 2 of: unilateral, throbbing, moderate/severe, aggrivated by physical exertion
not attributable to other causes
Triggers for migraines are
CHOCOLATE hangover orgasm cheese oral contraception lie in/destressing alcohol exercise
Management of migraines
firstly if sudden onset, exlude thunderclap
education on avoiding triggers
prevention by B blockers, Proplanolol or Botulinum
migrane rescue treatment by triptans (seritonin receptor agonist), NSAIDs and Antiemetic
Tension headache features
Commonest type of headache.
30 mins to 7 days.
2 of the 4: Bilateral, Mild/Moderate, Tight banding (not throbbing), not aggravated by physical exertion
No nausea/vomiting or aura
either photophobia or phonophobia or neither but not both.
if occurs 12 in a year considered chronic
A sign is scalp tenderness
Triggerst of tension headache
MCSCOLD Missed meals conflict stress clenched jaw over exersion lack of sleep
Precipiants of tension headache
worry, noise, concentration visual effort
commonest cause of tension headache
medication overuse
management for tension headache
education, avoiding triggers
NSAIDs and analgesic withdraw.
massage, ice pack
Cluster Headache Features
rapid onset of very severe headache, usually in one eye causing bloodshot eye or watery. miosis, ptosis, rhinorrhea.
always unilateral.
occurs at any age, unknown cause
get attack everyday for 4-12 weeks then a few months to a year of then back again
Diagnostic criteria for cluster headache
at least 5 attacks,
occurring at least one a day or at max 8 per day
V/Severe unilateral pain, suborbital orbital or temporal
lasts 15-180 minutes
accompanied by ipsilateral autonomic features or restlessness
management for cluster headache
100% oxygen for 15 minutes an sumatriptans
Prevention for Cluster Headache
Verapamil (CCB), lithium
Trigeminal neuralgia diagnostic criteria
occurs in Trigeminal nerve lesion, doesn’t radiate further, usually maxillary or mandibular
ha 3 of the following:
sudden recurring, lasting seconds to minutes
severe intensity
electric shock, stabbing, shooting,sharp
precipitated by stimuli of moving mouth, talk eat, clean.
Trigeminal neuralgia Causes
Primary idiopathic.
relating to age
secondary: skull abnormality, malignancy, MS
Trigeminal neuralgia Management
MRI, to identify if other cause, tumour etc.
Carbamazepine or gabapentin, (anticonvulsants)
surgery, microvascular decompression via gamma knife
whatmakes you think of secondary headache
over 50 years old with a new headache, jaw claudication (GCA). fever stiff neck (meningitis) papillodema, raised ICP headache. previous cancers. weakness that persists after headache (encephalitis or malignancy) cognitive decline.
thunderclap pattern
What is thunderclap headache.
Headache that comes on rapidly. reaches maximum severity in seconds. nausea and vomiting
sudden onset, severe, N&V. due to SAH
what is management of suspected secondary headache
CT Scan to identify cause
what is chronic idoioathic cranial hypertension and how to treat it
Raised ICH headache for no reason other than obesity and drugs.
Usually female. Young 20s
treat with diuretics
Remember obese girl with leopard print top with her mum in hallamshire
types of stroke and commonest
Ischaemic, commonest
hemorrhagic
SAH
Stroke in ACA
gait ataxia. leg and trunk weakness and sensory loss. akinetic mutism. loss of bladder control (incontinence), Dysarthria
Stroke in MCA
Unilateral weakness and sensory loss. facial droop aphasia, dysphagia
hemianopia
commonest site for stroke
Stroke in PCA
Homonymous hemianopia with macular sparing
visual agnosia
prosopagnosia
Stroke in Brainstem
which artery supplies this
stroke in PCA and Basilar. total paralysis but cognitive function and sensory from eye intact. locked in syndrome. consciousness and cognition intact
Stroke in lenicular region
which artery supplies this
Internal capsule is MCA supplied
Full contralateral hemiplegia, dysarthia, dysphagia
risk factors for stroke
which ones are for hemorrhagic- the first 2
Hypertension- largest smoking hyperlipidemia DM Family History Obesity previous TIA Heart Defects Carotid stenosis and bruti
what are the causes of ischeamic stroke and where do they come from
Usually thromboemboli from Common carotid, internal carotid, vertebral and subclavian.
1 in 5 strokes of those under 40 is dissection
causes of hemorrhagic stroke
severe hypo or hypertension
raised ICP
Polycythemia rubra vera
Investigations for Stroke
CT/MRI,
can do ECG to see if there is a cause, AF?
Ischaemic stroke management for the Clot.
within 4.5 hours: Thrombolytic therapy, Alteplase. ( +aspirin 24 Hrs, +LMWH, +further Investigations and prevention) (potential for stent retrieval - Endovascular Intervention)
After 4.5 hours: LMWH + Aspirin
ischaemic stroke further investigations
ECG,
Carotid doppler
CXR- heart enlargement
bloods- look for anemia, vasculitis, Polycythemia
Ischemic stroke further management for patient (prevention, conservative)
statins, better control of hypertension. diabetes, dual antiplatelet. if due to AF then give warfarin
surgery to remove carotid plaque (internal carotid endarterectomy
Conservative, Speech therapy, Occupational therapy, Physio
stop smoking and exercise
Swallowing assessment
Intracranial hemorrhage management
control ABC,
Surgery, Remove haematoma, surgical clipping stop all risk factors, control hypertension no more than 20% change
Stop antiplatelets, anticoagulants. normalise INR
look for signs of conning like hydronephrosis
SAH presentation
Thunderclap headache
sudden onset very severe, usually occipital
nausea and vomiting
lack of consciousness
SAH Investigations
CT Scan diagnostic
Can do CSF analysis
SAH complications
bleeding causes hydrocephalus
can lead to cerebral ischemia or rebleed cause death.
signs of SAH
Neck stiffness, kernegs sign
focal neurological deficit
Cause of SAH
ruptured berry aneurysm
risk factors for SAH
Smokers alcohol hypertension post menopause family history bleeding disorders
Management for SAH
control hypertension 20%
Dexamethasone- swelling
nimodipine - CCB reduce spasm and ischemia
what is a TIA
same as a stroke but the clot leaves on its own and symptoms clear within 24 hours
specific TIA sign
Amaurosis fugax- dark curtain coming over eye
causes of TIA
Thromboembolism from carotid or AF
Investigations in TIA
Done IOT find cause of TIA
MRI, Carotid doppler, ECG
Management of TIA
Avoiding risk of stroke
hypertension control, diabetes, statins, smoking, exercise, diet, dual antiplatelet
carotid endarterectomy
tool used to see urgency of referring TIA patient
ABCD2, predicts when next stroke will be and urgerncy to refer to specalist Age>65 1 Blood pressure>140/90 1 clinical unilateral weakness 2 speech and no weakness 1 Diabetic 1 Duration of symptoms less than 1 hour 1 more than hour 2 if score more than 4 then see within 24 hours. all TIA to be seen in 7 days
tool used to asses stroke risk in AF Patient
CHADSVASC2 congestive heart failure 1 hypertension 1 age>75 1 diabetes 1 stroke or tia 2 vascular disease (prior MI, PVD) -1 age >65 1 sex -female 1 9/9= 15 % change of stroke per year
Cardinal features of parkinsons
rigidity
resting tremor
bradykinesia - less blinking small writing little steps, shuffling gait
postural instability
Asymmetrical
causes of parkinson’s disease
idiopathic parkinson's disease, commonest trauma drug induced encephalopathy wilsons disease
Pathophysiology of parkinson’s disease
Degeneration of substantia nigra dopaminergic receptors- cant activate basal ganglia
investigations and diagnosis of parkinson’s disease
Clinical and history
DAT Scan- dopamine transporter scan confirmatory
management of parkinsonism
counciling, MDT approach, physio, parkinsons nurse,
Levodopa (co-careldopa)
MOAD/CMT inhibitors (second line)
surgery- ablation to subthalamic nucleus
manage depression
Complications of parkinsons
Depression dementia resistant to Ldopa psychosis autonomic features, constipation, ED
what does a broad based gait indicate
what are other features of this disease
Cerebellar disease, intention tremor normal tone DANISH dysdiadochokinesis, dysmetria ataxia nystagmus intention tremor scanning dysarthria/ slurred speech (jerky speech) hypotonia/ hyporeflexia
what signs would make you exclude a Parkinson’s diagnosis
Early dementia,
symmetry
early falls
early autonomic features, incontinence
these are suggestive of normal pressure hydrocephalus - Idiopathic CSF Build up which is drained surgically
what are the features of an essential tremor
what are the causes, investigations and treatment of this
no little rest tremor
no increased tone or dyskinesia
postural and action tremor
Structural abnormality, CT and Physio and B blockers
what is huntington’s disease
Neurodegenerative disease caused by malfunction in huntingtin gene. causes neuronal cell atrophy.
Pathophysiology and progression of huntington’s
Starts of with increased dopamine production and atrophy of the indirect pathway. this causes less inhibition and the huntingtons cardinal signs (chorea and Hyperkinesia).
as huntington’s progresses, the direct BG pathway is lost leaving only the inhibitory function of the basal ganglia to be active, causing hypokinesia
atrophy of the brain also causes psychiatric problems.
Presentation of huntington’s
Cardinal- Chorea- hyperkinesia
dementia
psychiatric problems/ personality change
other signs: abnormal eye movements, chorea, ataxia, rigidity (late sign), eventually develops to parkinsonism signs
Diagnosis of huntington’s via genetic screening
36 CAG triplet repeats
Huntington’s genetic features
Autosomal dominant
100% penetrance,
gets more and more repreats with every generation - starting earlier (anticipation)
Huntington’s treatment
Neuroleptics- Dopamine receptor blockers, (promazine Hydrochloride)
depression- SSRIs, Sertraline
family screening
MDT, Physio, Occupational Health, Huntington’s nurse, social care
what is Multiple Sclerosis
Chronic Inflammatory demyelinating disease of the CNS
Prevalence of MS
average age of onset
commonest cause of neurological deficiency in adults
average onset 20-40 Y O
0.1% of population in UK
Risk Factors and of MS
Risk increases the further you get from the equator being female vit D deficiency family history sanitation diet race, commoner in caucasian and white
Pathophysiology of MS
demyelination plaques due to T cell mediated inflammation. plaques most commonly in optic and periventricular regions.
as inflammation occurs, relapse. as it subsides, remyelination it remittes
What are the different patterns of presentation of MS
Relapsing remitting, 80% most common
Primary Progression
secondary progression- starts relapsing remiting and becomes progressive
begine, only has a few episodes
Presenation of MS
what are common symptoms and a MS specific Sign
like a stroke, but gets better then worst again, can happen anywhere in CNS, optic, spine, cerebellum, brainstem
Epilepsy and trigeminal neurlagia are common
can cause depression or dementia
+ve Uhthoffs phenomenon
Differential diagnosis Of MS
on first presenation could be stroke, Betchets disease
SLE (look for extremly +ve family history)
what is uhthoff’s phenomenon
MS patients symptoms get worst after putting them in a hot bath, due to heat slowing down conduction
Diagnostic criteria for MS
Mcdonald’s diagnosis
needs to have 2 or more episodes that are disseminated in time, and disseminated in lesion space
exclude all other causes
Investigations for MS
MRI- tries to identify demyelinating plaque or exclude other causes
CSF analysis - shows inflammatory markers in CSF
No inflammation in bloods
Management of MS
Conservative: Physio, OH, Neurologist, MS Nurse speech, counciling, psychological counseling.
education on lowering stress and uhthoff’s.
symptoms elevated by coolness
Tremor treated by B blockers
SSRI sertraline, for depression
Disease modifying treatment is IV methylprednisolone steroids.
prevention of onset, B Interferons.
Immunosuppression and monoclonal antibodies
what is meningitis
Inflammation of the meningies
What are the causes of meningitis,
Viral, Bacterial, fungal or parasite
most common Streptococcus pneumoniae
less common but also prevalent: niesseria meningitidis
Paraneoplasia, meningioma, Drug Induced, Autoimmune (SLE)
Which meningies are affected in meningitis
Pia and Arachnoid
Presentation of meningitis
Triad:
Pyrexia,
Neck Stiffness
Headache
other: Photophobia, vomiting, malaise, rigiors
can develop into sepsis
loss of consciousness, focal seizures
Signs of meiningitis
petechial rash
Kernig’s sign- flex hip and knee then extend knee, pain= Kernig’s sign +ve
Brudzinski signs- knee and hip flex spontaneously when neck is flexed
What else causes Kernig’s signs and Neck stiffness
SAH
management for meningitis pre hospital
IM/IV Benzylpenicillin
Management for Meningitis
IV Cefotaxime (+Ampicillin if over 55)
Steroids, IV Dexamethasone
Investigate further
asses sepsis
Investigations and Diagnosis for meningitis
Bloods ESR CRP Definitive: lumbar Puncture, CSF MS & C if gram +Ve, strep pneumoniae gram -VE, neisseria meningitidis (notifiable) CXR TB LP is CI in raised ICP or Pectinal rash
Who’s at risk of meningitis
Students travelers
immunocompromised
what is the causing agent of Encephalitis
Herpes simplex, commonest cause
other:
Herpes zoster, HIV Measles and Mumps
Presentation of encephalitis
History of general unwell, flu like symptoms
day of presentation= altered GCS Fever Seizures Confusion memory loss
Investigation of Encephalitis
MRI exclude other
EEG- diagnostic
blood cultures and lumbar puncture MC&S to identify cause
Treatment of Encephalitis
Treat causative agent,
Antiviral, IV acyclovir
what are the different kinds of seizures
Partial/ focal- can be simple or complex ( consciousness)
partial can develop into generalised, secondary generalised
primary generalised - can have absent, myoclonic (isolated jerky movement) that develops into tonic clonic
what are preictal features
symptoms that occur before seizure, general feeling or auras, jamis vue, deja vu. commonly occurs before focal seizure (Temporal lobe)
what are Post ictal features and what are they indicative off.
Can have weakness, (todd’s palsy) resolves after a while, aphasia, dysphasia. these are signs of focal seizure ( Frontal lobe)
features of frontal lobe epileptic features
Partial seizure, consciousness retained, enter jacksonian march or seizure, where they are fully aware of what they are doing but have no control.
develops todd’s palsy afterwards, Hemiparesis that resolves within 2 days
Features of a temporal lobe epileptic seizure
partial seizure, can be conscious or unconscious. gets automatism complex, (start doing things automatically) no memory retained. dysphasia, lip smacking, de ja vu jamai vue. usually tend to have isolated muscle seizures. move only one limb.
can develop into secondary generalised seizure.
has features afterwards, or other post ictal features
Features of a generalised seizure
can start of with myoclonic isolated muscle movements, can start of as partial then develop. develops into tonic clonic seizure.
Length of seizures,
30 seconds -120 seconds. generally under 3 minutes
examination a=of a seizure, things you can ask witness
How long did the seizure last
what was the character of the seizure, how did it change, phases of the seizure. the speed of convulsions.
if incontinence.
Sequence of events of seizure.
any post ictal signs they have noticed like dysphasia
Examination of a seizure, what would you ask the patient
what were you doing before seizure
did you notice any preictal symptoms, deja vu jamais vu, auras, general feeling.
did you retain consciousness during the seizure. do you have monory of what happened
post ictal features, dysphasia, todd’s Palsy.
does their tongue hurt, indication of tongue biting.
incontinence during seizure
Investigations of a seizure
any seizure needs to have CT/MRI witness statement EEG also try to exclude other causes, ECG, BP, Hypoxia, Pseudoseizure due to stress. CXR, TB, Sarcoidosis, SLE. Electrolytes
commonest cause of seizures
2/3. Idiopathic generalised epilepsy, usually familial.
other causes of seizures
pseudoseizure - stress related
Focal epilepsy, (secondary) due to anything pressing on brain, Tumour. SAH, Meningitis
metabolic- low or high Na, low glucose, Low Ca, Uremia.
Low BP, syncope. heart problems
TB, Sarcoidosis, SLE
Management of seizures
conservative
education on potential triggers, alcohol, substance, stress. medications
education on maintaining safety, driving. avoid baths, locking doors.
Pharmacological management of seizures
antiepileptic drugs- carbamazepine - for tonic clonic, and partial seizures
sodium valproate- for all other kinds
Surgical management of seizures
Vagus nerve stimulation,
surgical- hippocampal section if sclerosis
corpus callosum section
Prognosis of epilepsy
majority are seizure free 2 years after starting meds
what is the blood supply if the spinal cord
Vertebral arteries- anterior spinal artery
Intercostal arteries
lumbar vessels
spinal cord landmarks
from medulla till L1/2 then conus medullaris and it extends as cauda equina
what are the principle features of spinal cord compression
spastic hemiparesis, or tetra or quadra. (weakness and stiffness)
radicular pain at level of compression (pain radiating along nerve root
sensory loss below compression
if compression above S234 causes retention and constipation ( detrusor and sphincter contract at the same time
what are the causes of spinal cord compression
spinal neoplasm
Disc and vertebral lesions (trauma, osteoporotic fracture
TB- Pott’s disease
epidural hemorrhage or hematoma
What are the spinal cord neoplasms
Extradural- metastatic
Extrameduallary- meningioma
Intramedullary- glioma
Investigations for spinal cord compression
Gold standard is MRI
Investigate other causes
managment for spinal cord compression
surgical decompression, removal of tumour.
if malignant then chemo+radiotherapy
what is cauda equina syndrome
cord compression between L2 and S5
causes of cauda equina syndrome
same as SP compression. common iatrogenic from LP. (epidural hematoma) this is why LP is CI in raised ICP
presentation of cauda equina syndrome
saddle anesthesia, severe back pain, incontinence, sciatica, gait disturbance
Management of cauda equina syndrome
laminectomy- remove vertebra to allow for decompression.
causes of CN 7 palsy
Idiopathic Bell's palsy 70% ramsay hunt syndrome- herpes zoster Lyme disease meningitis stroke tumour MS Diabetes Parotid tumour
CN7 Palsy presnetaion
Unilateral facial weakness, speech difficulty,
no taste in ant 2/3 of tongue
sound hypersensitivity due to stapedius not working.
risks and associations with Bell’s palsy
unknown onset during the night,
increased risk in pregnancy
diabetes
Investigations and diagnosis of bells palsy
Exclude other causes. MRI, cultures serology for lyme and ramsay hunt
Management of bells palsy
if present within 3 days. prednisone
if afterwards corticosteroids.
potential surgery to close eyelid
Prognosis of Bell’s palsy
if paresis most recover in a few weeks
if plegia, 80% recovery
what is the commonest neuropathy
Sensory motor chronic neuropathy due to DM
What is a sign of brain tumour
Papilloedema
What are neuroleptics, what do they cause and when do you use them
antipsychotic class, used in huntington’s sice dopamine antagonist (levomePROMAZINE)
cause drug induced parkinson’s
Treatment for essential tremor
Physio and B blockers
Subdural hemorrhage Presentation
Altering consciousness and GCS Physical or intellectual slowin Sleepiness headache personality changes
Subdural hemorrhage cause
Most are from trauma a while ago, minor trauma
can occur with falls in epileptics r alcoholics
elderly are susceptible
Subdural hemorrhage Investigations
CT / MRI showing clot or midline shift (Crescent shaped)
Subdural hemorrhage Management
1st line: irrigation/evacuation Blurr twist
2nd: craniotomy
Signs of Subdural hemorrhage
Increased ICP
Seizures
focal neurological features
Extradural haemorrhage cause and pathophysiology
often occurs after immense trauma causing fracture of temporal or parietal bone causing a Laceration in meningeal artery
or trauma leading to a tear in venous sinus
Extradural haemorrhage Presentation
Deteriorating consciousness after head injury
Initially not producing anything but gets worse progressively
few hours later ICP rises
Vomiting headache
Low GCS
Seizures
Hemiparesis plus brisk reflex (hyperreflexia)
Ipsilateral pupil dilates
progresses to bilateral weakness
Breathing difficulty (due to compression)
Investigations of extradural Haemorrage
CT Shows haematoma, lens shaped, more rounded
X ray may show fracture
Management of Extradural haemkrrage
Stabilize and transfer to neurosurgery for clot evacuation
Airway care
Mannitol to reduce ICP
