Neuro Flashcards
UMN vs LMN lesion features
LMN shows PERIPHERAL NS symptoms:
muscle wasting, fasciculations, reduced tendon reflexes and tone,
forehead involved if CN VII involved in lesion,
signs are on the same side as the lesion, hypotonia,
FOCAL pattern of weakness (only specific muscles innervated by nerve)
UMN shows CENTRAL NS symptoms:
increased tone and reflexes, upgoing plantars (Babinski +ve),
if facial weakness then forehead is spared,
signs are on OPPOSITE side of lesion,
No muscle wasting,
Extensor planter response present
PYRAMIDAL pattern of weakness seen: extensor muscles affected but flexors are not etc. eg in STROKE
UMNs mainly form sensory and intermediate neurons with inhibitory effect on LMNs reflexes, therefore damage to an UMN or its connections with LMN will EXAGGERATE the reflexes
ACh, function and examples of malfunction
Noradrenaline function and examples of malfunction
ACh:
Enables muscle action, learning and memory
In Alzheimer’s, ACh producing neurons deteriorate
NA:
Helps control alertness and arousal
Undersupply is linked to depressed mood
Dopamine functions, examples of malfunctions
Influences movement, learning, attention and emotion
Excess dopamine receptor activity is linked to schizophrenia
Starved of dopamine, the brain produces the tremors and decreased mobility of Parkinson’s
Serotonin (5HT) function and examples of malfunction
Affects mood, hunger, sleep and arousal
Undersupply is linked to depression
GABA and glutamate function and examples of malfunction
GABA:
Major inhibitory neurotransmitter
Undersupply is linked to seizures, tremors and insomnia
Glutamate:
Major excitatory neurotransmitter involved in memory
Oversupply can overstimulate brain producing migraines or seizures (which is why some people avoid MSG monosodium glutamate in food)
Meningitis
Inflammation of the inner meninges (mostly pia and arachnoid) of the brain and spinal cord
Route of transmission: direct (aerosol, droplet secretion, direct contact with secretions, ear infections, nasopharynx, cranial injury), via the blood (septicemia) or viral meningitis (most common)
Bacterial meningitis is less common but high mortality especially high risk in infants
Cause varies with age, vaccination status (less than 4 years and unvaccinated) and other medical conditions
Meningococcus is most common cause of bacterial meningitis in UK (B, C subtypes)
In UK, syphilis, TB and fungal infections are rare causes
Klebsiella P account for most causes of hospital acquired meningitis (nosocomial infection)
Common causes:
Meningococcus (neisseria meningitidis)
Pneumococcus (streptococcus pneumonia)
Haemophilus influenzae
Types of meningitis
in addition to common classification according to microorganism cause
Aseptic meningitis - CSF has cells but is gram -ve and no bacteria can be cultured include viral and fungal causes
Non-infective meningitis (systemic disease) - inflammation due to infiltration of the meninges, such as malignant cells (leukemia, lymphoma) or rheumatological conditions (sarcoidosis or SLE)
Meningitis presentation
Very general in children: headache, fever, vomiting, malaise
Headache
Neck stiffness (nuchal rigidity)
Fever
Muscle ache/joint pain
Vomiting
Kernig’s sign: inability to fully extend knee when hip is flexed 90 degrees
Brudzinski’s sign: passive flexion of neck causes flexion of both legs and thighs
Papilloedema - swollen optic disc due to increased intracranial pressure
In meningococcal septicaemia - non-blanching petechiae and purpuric skin rash and signs of shock (this is a LATE sign due to septicaemia being present usually day 5 onwards)
Meningitis investigations
Diagnostic: lumbar puncture and laboratory CSF analysis
Bloods: FBC, CRP, blood cultures, blood glucose, ABG/VBG
KFT
Urine cultures
CXR (lung infections or abscesses)
CT (sometimes before LP) to exclude high intracranial pressure however NICE recommends clinical assessment NOT CT for this
Lumbar puncture complications and CIs
LP complications:
Coning (cerebral herniation)
Introduction of infection into CSF
CIs:
Local skin infection
Bleeding problems or anticoagulant therapy
Signs of spinal cord compression/pathology
Papilloedema or other signs of raised intracranial pressure
Suspicion of intracranial or cord mass
Congenital neurological lesions in lumbosacral region
Must have consultant present for LP with any CIs:
Raised ICP or reduced fluctuating loss of consciousness
Altered consciousness (GCS <9)
Focal neurological signs
Relative bradycardia and HTN
Abnormal posture
Unequal, dilated or poorly responsive pupil
Papilloedema
Shock
Coagulation abnormalities or therapy or platelet count <100x109/litre
Local superficial infection at LP site
Respiratory insufficiency in children
Normal CSF in adults
White and colourless
WBC: 0-5 cells/uL
No neutrophils, primarily lymphocytes
RBCs: 0-10/mm3
Protein: 0.15-0.45g/L (or <1% serum protein concentration)
Glucose: 2.8-4.2mmol/L (or >60% plasma glucose concentration)
Opening pressure: 10-20cm H2O
CSF overview in meningitis
Viral: clear, white cells high 5-1000, predominantly lymphocytes, normal RBCs <10, normal/high protein 0.4-1, normal glucose, normal/slightly high opening CSF pressure
Bacterial: cloudy and turbid look, very high white cells 100-50,000, neutrophils (PMN) predominately (some can cause leukocytes), high protein >1, decreased glucose <40%, high opening CSF pressure
TB meningitis: cloudy and viscous, increased white cells <500, mostly lymphocytes, very high protein 1-5, decreased BG <30%, high opening CSF pressure
FUNGAL MENINGITIS: clear/cloudy Elevated opening pressure Elevated WBC (10-500) Low glucose Elevated protein Gram stain positive Most likely causative organisms: cryptococcus neoformans and candida
Meningitis management
Urgent: all suspected meningitis cases are medical emergencies needing immediate hospitalisation
Suspected with rash - empirical antibiotics IM/IV benzylpenicillin (CI in severe allergy, give cefotaxime or ceftriaxone if allergy) blind therapy 1st line - targets meningococcal strain most common in UK
2nd choice antibiotics given when blood/CSF culture results are back (adult <50 - cefotaxime or ceftriaxone for 7-10 days, adult >50 cefotaxime or ceftriaxone + amoxicillin or ampicillin for 7-10 days)
Suspected without rash - urgent hospitalisation NO ANTIBIOTICS unless urgent transfer not possible
Suppurative treatment - analgesia, antipyretics, VI fluid (viral cause)
Identify signs of shock and sepsis an treat as needed
Dexamethasone (add on treatment before or with antibiotics within 12 hours)
Close contact prophylaxis - ciprofloxacin or rifampicin or IM ceftriaxone. People who have had prolonged close contact with case in household setting during 7 days before onset of illness (healthcare workers don’t need unless direct exposure of mouth/nose to infectious droplets with patient with <24 hours antibacterial treatment)
Notification of health protection unit (notifiable disease)
Meningitis complications
Much higher in meningococcal septicaemia (up to 57%)
Cerebral infarction in 1 in 4 people with bacterial meningitis
Neurological complications: hearing loss (higher in infants and children), seizures, cognitive impairment, motor deficits, visual impairments
Hydrocephalus
Learning difficulties
Encephalitis
Inflammation of the brain
Mostly caused by viral or post-infectious due to autoimmune disease
Causes:
Viral: HSV-1, CMV, EBV, VZV, HIV, measles, mumps, rabies, enterovirus
Bacterial: all causes of bacterial meningitis including TB, mycoplasma and listeria
Fungal and parasitic infections
Encephalitis presentation
Fever Headache Neck stiffness Vomiting Altered consciousness Convulsions Focal neurological signs Signs of raised intracranial pressure Psychiatric symptoms
Encephalitis investigations
CSF analysis for HSV-1 or 2, VZV and enteroviruses: usually shows moderate protein increase, raised lymphocytes, CSF/glucose ratio normal
FBC, blood cultures, renal function, U+Es, LFTs, glucose, ESR, CRP
CT scan for lesion/tumour, raised ICP (DOES NOT RULE OUT DIAGNOSIS)
MRI scan to detect demyelination and oedematous changes
Encephalitis management and complications
Urgent hospital admission
Parenteral antibiotics if suspected meningitis (IV/IM benzylpenicillin)
Immediate treatment with IV acyclovir (improves prognosis) +/- antibiotics to treat secondary bacterial infection
Careful IV fluid administration as this can worsen cerebral oedema
Complications: Mortality 70% in 7-10 days if untreated SIADH Disseminated Intravascular Coagulation Epilepsy Complications are usually linked to affected area of brain
Tuberculosis meningitis
Pathology:
Haematogenous spread eg miliary TB, foci of infection in brain and spinal cord
Foci can enlarge forming tuberculomas - foci rupture leads to meningitis
Active TB:
Containment by immune system by T cells and macrophages is inadequate
TB contagious
Either primary infection or reactivation of latent TB
Latent TB:
Granuloma formation prevents bacterial growth and spread - persistent immune system contaminant
Skin or blood testing (TBT, IGRAS) are positive - infection exists but sputum/CXR are normal - patient is asymptomatic and non-infectious
TB meningitis risk factors and presentation
Immunosuppression
HIV/AIDS
Alcoholism
Age <3 YO
Presentation: Headache Meningism Confusion FND Seizures Systemic symptoms: fever, night sweats, anorexia, weight loss and malaise
TB meningitis investigations
LP and CSF analysis: leukocytosis, raised protein, CSF plasma glucose <50%,
NAAT in CSF
AFB stain
PCR and culture
Serologic HIV test
CT/MRI may show hydrocephalus or Tuberculomas
general testing - tuberculin skin testing or IGRAS testing (more sensitive for BCG vaccination)
Management of TB meningitis
Rifampicin 2 months intensive 4 months continuation - p450 inducer: warfarin, calcineurin inhibitors, oestrogen etc. body secretion can coloured orange or red, altered liver function
Isoniazid 2mths intensive 4mths continued - risk of peripheral neuropathy and hepatitis, give with prophylactic pyridoxine,
Pyrazinamide 2 mths intensive - hepatotoxicity risk, measure eGFR before
Ethambutol 2mths intensive - may cause colour blindness and poor visual acuity must check visual acuity before starting and monitor monthly and eGFR
Shingles
VZV varicella zoster virus, form of herpes virus
In children: respiratory droplets containing virus enter lungs and incubate for 14-21 days. Invasion to respiratory mucosa, disseminates via mononuclear cells to skin. Virus containing vesicles causes CHICKEN POX, remains dormant in sensory nerve roots for years
In adults: reactivation of VZV but this time is limited to a dermatome of the skin = SHINGLES
Shingles is less contagious than varicella - household transmission rate is 15%
Blood test for antibodies can confirm is ever had chickenpox before
Those exposed to VZV if never had chickenpox before will get chicken pox no matter what age, but those who have HAD chickenpox will get shingles if reexposed
Presentation of shingles
Painful, burning, numbness in area in prodromal period
Few days later shows macular vesicular rash in SINGLE DERMATOME
Most common sites: lower thoracic dermatomes and ophthalmic division of trigeminal nerve V1 (ocular shingles)
Rash is still infectious until lesions dry and become crusted
Complications and management of Shingles
Post-herpetic neuralgia can be severe for years: most common complications, 10-20% cases of HZ (up to 30% in elderly). Pain lasting for >30 days from onset of lesions. Symptoms include constant or intermittent stabbing or burning pain, allodynia (pain induced by non-painful stimulus), hyperalgesia (severe pain from mildly painful stimulus) and intense itching. Amitriptyline is very effective at managing pain
Ramsay hunt syndrome (facial palsy with auditory involvement)
Immunosuppression can show skin involvement affecting multiple dermatomes
Management:
IV acyclovir for immunosuppressed, severe/disseminated disease (including ocular)
Pregnant women - oral acyclovir (if >20 weeks gestation) can use IV in severe or progressive maternal or neonatal infection as is not embryotoxic and can improve outcome significantly
Prevention: vaccination 9Zostavax) for those >50 YO to prevent recurrence of shingles or zoster immune globulin (VZIG) for pregnancy if VZ antibody negative or in neonates - does not prevent infection but attenuates the disease if given within 10 days
Cranial nerve VII
Facial nerve
Origin from Pons and medulla
Innervation anterior 2/3rds of tongue, facial muscles, scalp, ear and neck
Function to control facial muscles, motor limb of blink and corneal reflex, secretion of salivary and lacrimal glands, sensation of taste, anterior 2/3rd of tongue
LMN palsy and evaluation
Acute LMN palsy can present at any age but mostly seen at ages 15-60 years affecting both sexes equally
Rapid onset of unilateral facial paralysis
Clinical evaluation:
Motor function: observe facial symmetry, flattening of nasolabial fold, ask patient to wrinkle forehead, puff cheeks and smile. Show teeth, close eyes against resistance and whistle
Wrinkle forehead - frontalis
Close eye - orbicularis oculi
Purse lips - buccinator muscle
Show teeth - orbicularis oris
May have aching pain below ear or in mastoid area which may suggest middle ear or herpetic cause
May be hyperacusis (heightened sensitivity to perceived sounds)
Bells palsy
LMN lesion indicative of damage to motor nucleus or peripheral component
Patient can’t wrinkle forehead as final common pathway to muscles is destroyed
Lesion must be either in pons or outside brainstem
Sudden onset, ipsilateral weakness or paralysis on one side
Almost always unilateral and can be recurrent
Most common cause of acute LMN facial palsy
As a result of inflammation of facial nerve in canal due to viral infection (HSV1 or VZV) is the most common cause
Bells palsy features
Eyebrow droops, frowning or raising eyebrows is impossible
Eye cannot be closed; when asked to close eyes and show teeth, eyeball rotates upwards and outwards (Bell’s phenomenon)
Lower lid is everted. Tear production (lacrimation) is decreased
Mouth droop and patient dribbles
Bells palsy managament and prognosis
Reassurance - the majority of cases resolve spontaneously within 3 weeks
Prednisolone given to those over 16 YO presenting within 72 hours onset for 10 days
Antivirals NOT recommended in UK
Eye care (lubricating drops +/- ointment
Referral to ophthalmologist if further functions affected for Botulinum toxins or surgery if needed
Prognosis and complications:
70% fully recover
16% significant complications
5% develop severe facial asymmetry, gustatory lacrimation, inadequate lid closure, brow ptosis, drooling or hemifacial spasms
Focal neurological deficits
FND is a focal problem with the nerve, spinal cord or brain function
Affects a specific location/function such as the left side of the face, right arm or even small area such as the tongue. Speech, vision and hearing problems are also considered focal neurological deficits
Frontal lobe FND signs
Usually involve motor system and may include special deficit types depending on which part of the frontal lobe is affected
Unsteady walking
Muscular rigidity, resistance to limb movement (hypertonia)
Paralysis of limb (monoparesis) or larger area on one side of body (hemiparesis)
Paralysis of head and eye movements
Inability to express oneself linguistically, expressive aphasia (Broca’s aphasia)
Focal seizures which can spread adjacent areas (Jacksonian seizure)
Grand mal/tonic-clonic seizures
Changes in personality - disinhibition, inappropriate jocularity, rage, loss of initiative and concern, apathy etc
Frontal release signs: reappearance of primitive reflexes such as snout reflex, grasp reflex and palmomental reflex
Unilateral loss of smell (anosmia)
Parietal lobe FND signs
Usually involve somatic sensation and can include
Impaired tactile sensation
Impaired proprioception (postural and passive movement sensation)
Sensory and visual neglect syndromes - inability to pay attention to things in certain parts of sensory or spatial environment even as extreme as denial of a limb
Loss of ability to read, write or calculate (dyslexia, dysgraphia or dyscalculia)
Loss of ability to identify objects based on touch (astereognosis)
Temporal lobe FND signs
Usually involve auditory sensation and memory
Deafness without damage to structural (cortical deafness)
Tinnitus, auditory hallucinations
Loss of ability to comprehend music or language (sensory aphasia - Wernicke’s aphasia)
Amnesia, memory loss (long or short term)
Other memory disturbances (deja vu)
Complex multimodal hallucinations (these display complex forms and fill the entire visual field unlike occipital signs)
Complex partial seizures (temporal lobe epilepsy)
Occipital lobe FND signs
Usually involve visual sensation
Total vision loss (cortical blindness)
Loss of vision with denial (Anton’s syndrome)
Loss of vision on one side of visual field of both eyes (homonymous hemianopsia)
Visual agnosias ie inability to recognise familiar objects, colour or faces
Visual illusions such as micropsia (objects appear smaller) and macropsia
Visual hallucinations, displaying elementary forms such as zig zags and flashes in one half of visual field only for each eye
Cerebellar FND signs
Usually involve balance and coordination
Unsteady and clumsy motion of limbs or torso (ataxia)
Inability to coordinate fine motor activities (intention tremor) eg past pointing (pointing beyond the finger in finger nose test)
Inability to perform rapid alternating movements (dysdiadochokinesis) eg rapidly flip the hands
Involuntary left to right eye movements (nystagmus)
Brainstem and spinal cord FND signs
Brainstem signs:
Involve host of specific paralysis with contralateral loss of pain sensation
Spinal cord signs:
Generally involve unilateral paralysis with contralateral loss of pain sensation
Headaches history taking
Location Severity Character Associated symptoms Autonomic symptoms Relieving and exacerbating factors Number of episodes Duration of episodes Frequency of episodes Age of onset Triggers Analgesic use Family history Red flags
Red flags for headaches
Fever, photophobia or neck stiffness (meningitis or encephalitis)
New neurological symptoms (haemorrhage, malignancy or stroke)
Dizziness (stroke)
Visual disturbance (temporal arteritis, glaucoma, pituitary adenoma)
Sudden onset occipital headache (subarachnoid haemorrhage)
Worse on coughing or straining (raised intracranial pressure)
Postural, worse on standing, lying or bending (raised intracranial pressure)
Severe enough to wake from sleep
Vomiting (raised ICP or carbon monoxide poisoning)
History of trauma (intracranial haemorrhage)
Pregnancy (pre-eclampsia)
Primary and secondary causes of headaches
Primary: No structural or metabolic abnormalities: Tension headaches Migraines Cluster headaches Other primary headaches
Secondary:
Structural or metabolic abnormality:
Extracranial: sinusitis, otitis media, glaucoma, TMJ ds
Intracranial: SAH, vasculitis, dissection, CVT, tumour, abscess, meningitis
Metabolic disorders: CO2 retention, CO poisoning
Tension headaches
Very common and often suffer from both migraines and tension type heades (TTH)
Classically produce mild headache across forehead and in band-like pattern around the head with pressure behind the eyes and pericranial tenderness also often a symptom
Can last few mins to few days; often bilateral
Generally not activated by activity and not ‘severe’
Exact mechanism unknown
May be due to frontalis, temporalis and occipitalis muscles or neck muscles
Come on gradually and resolve gradually
Do NOT produce visual changes
Classification:
Infrequent: (<1 month)
Frequently (>10/month for 3 months)
Chronically (>15/month for 3 months)
Pathophysiology:
Trigeminal nerve supplying pericranial muscles, vessels and dura mater
Tension headaches are caused by abnormality in this nerve
Headaches associations and diagnosis
Associations: Stress Depression Alcohol Skipping meals Dehydration
Diagnosis: must have 2 of the following
No nausea or vomiting
Either photophobia or phonophobia NOT both
Not aggravated by movement
Management of headaches
Exclude serious causes of headache
Reassurance
Basic analgesia (rule out medication overuse)
Relaxation techniques and exercise, massage and ice packs
Hot towels to local area
Headaches occurring more than 2 days/week NICE recommends course of acupuncture first line or low dose amitriptyline 25-150mg ON 2nd line (4-6 months then withdraw slowly)
Secondary headaches
Similar presentation to tension headache but with clear cause
Produce a non-specific headache secondary to:
Underlying medical condition like infection, obstructive sleep apnoea, pre-eclampsia
Alcohol
Head injury
Carbon monoxide poisoning
analgesic headache
Caused by long term analgesia use
Gives similar non-specific features to tension headache
Secondary to continuous or excessive analgesia use
Withdrawal of analgesia important in treated the headache, although this can be challenging in patients with long term pain and those that believe the analgesia is needed to treat the headache
Hormonal headache
Related to oestrogen
Produce non-specific tension like headaches, tend to be related to low oestrogen
Often two days before and first three days of menstrual period
Around menopause
Pregnancy: worse in the first few weeks and improves in the last 6 months. Headaches in second half of pregnancy should prompt investigation for preeclampsia
Oral contraceptive pill can improve hormonal headaches
Cervical spondylosis
Common condition caused by degenerative changes in cervical spine
Causes neck pain usually made worse by movement but often presents with headache
Important to exclude other causes of neck pain such as inflammation, malignancy and infection as well as spinal cord or nerve root lesions
Cluster headaches
Rare type of headache caused by trigeminal autonomic cephalalgias (TACs): causes unilateral headache and autonomic features are present on same side as headache
Come as cluster of attacks and then disappear for a while (3-4 attacks a day for weeks/months followed by pain free period of 1-2 years)
Attacks can last between 15 minutes and 3 hours
Typically affects those aged 30-50
More common in smokers and adult males
Attacks can be triggered by alcohol, strong smells and exercise
Cluster headache presentation
Often described as most severe intolerable pain
Sometimes referred to as suicide headaches due to severity
Clusters last 1-2 months, remission for months or years
Lasting few mins to few hours and can occur several times a day
Typically unilateral located to one eye
Red, swollen and watering eye
Pupil constriction (miosis)
Eyelid drooping (ptosis) and oedema
Nasal discharge/rhinorrhoea
Facial sweating
Gets worse when lying down, often they pace the floor
Cluster headache management
Acute:
Check for red flags for secondary headache
Referral for neurology discussion
Triptans (sumatriptan 6mg subcut injection)
High flow oxygen for 15-20 minutes (can be given at home)
Prophylaxis: managed by neurology
Verapamil
Lithium
Prednisolone (short course 2-3 weeks to break cycle during clusters)
Can give injections into scalp of steroid and anaesthetic lasting few weeks to break cycle
Epilepsy
Umbrella term for seizure disorder when neurons are synchronously active
Recurring and unpredictable
Paroxysmal electrical discharges of neurons - temporarily impaired and send out sudden excitatory signals
Thought to be due to too much excitation or too little inhibition
Glutamate is main excitatory NT in brain and NMDA is main receptor
Some patients with epilepsy seem to have fast or longer acting activation of NMDA
Some patients have too little GABA inhibition due to dysfunctional GABA receptors leading to lack of inhibition
Can also be affected by brain tumours, brain injury or infection
Seizures and causes
Occur when there is abnormal electrical discharge in brain
Causes include: Sodium or glucose disturbances Infection (meningitis etc) Brain injury Electric shocks Brain tumours Drugs overdose Febrile seizures
Types of seizure
Generalised: both hemispheres affected Tonic-clonic Absent Myoclonic Tonic Infantile spasms/west syndrome Atonic
Partial/focal seizures: part of hemisphere affected, usually limited to part of cortex temporal lobe frontal lobe parietal lobe occipital lobe
Generalised seizures
both hemispheres of the brain affected
Patient will lose consciousness or awareness and may not remember the seizure
No warning of occurrence
Can begin as partial and spread to general.
Subcategories: tonic (stiff/fixed). Atonic (relaxed). Clonic (convulsions). Myoclonic (short muscles twitching only). Absence (lose and regain consciousness - appear ‘spaced out’)
Tonic-clonic is most common form (stiff then convulsions follow)
Tonic clonic seizures
(grand mal):
Initial tonic stiffening, may cry out then fall
Followed by clonic phase of synchronous jerking of limbs, should reduce in frequency over about 2 minutes
Eyes remain open
Patient may bite tongue
Urinary and/or faecal incontinence can occur
Patient may remain unconscious after awareness may return gradually
Postictal phase: drowsy and confused, irritable or depressed
Management:
First line sodium valproate
Second line lamotrigine or carbamazepine
Absence seizures
(petit mal):
Commonly start in childhood
Typically lasting only 10-20 seconds
Loss of awareness, show vacant expression, may see eyelids fluttering
Patient then returns to normal as though nothing happened
May happen several time a day and can be very short
Almost always a manifestation of generalised epilepsy
May start to experience other types of generalised seizures
Management:
Sodium valproate or ethosuximide
Myoclonic seizures
Abrupt involuntary jerks of the whole or part of the body
Can be very short
Typically occur in various forms of epilepsy but often in children as part of juvenile myoclonic epilepsy
Management:
First line sodium valproate
Lamotrigine, levetiracetam or topiramate
Tonic seizures and infantile spasms
Sudden increase in muscle tone
Patient becomes rigid and falls
infantile spasms:
West syndrome
Rare disorder starting in infancy at around 6 months old
Characterised by full body spasms
Poor prognosis - 1/3rd die by age 25 however 1/3rd are seizure free
First line management prednisolone or vigabatrin
Atonic seizure
‘drop attacks’:
Sudden loss of muscle tone
Causes patient to collapse and become very floppy
Don’t usually last more than 3 minutes
Typically begin in childhood
May be indicative of Lennox-Gastaut syndrome
Management:
Sodium valproate
lamotrigine
Partial of focal seizures
Only one hemisphere or lobe is affected, usually limited to part of the cortex in on hemisphere
Manifestation depends on part of the brain involved
Auras can accompany focal seizures
Subdivided into simple partial seizure where patient remains conscious, or complex partial with impaired consciousness
Important to rule out structural lesions
Usually rather brief
Simple partial: Remains conscious Small area of the brain affected Causes strange sensations for patient depending on lobe affected Doing strange things on autopilot Or jerking movements Usually aware of something happening to them Often remembers event Jacksonian march
Complex partial:
Impaired or loss of consciousness and responsiveness
Often do not remember the even
management:
- carbamazepine or lamotrigine
- sodium valproate or levetracetam
Temporal lobe seizures
Aura: epigastric sensation, olfactory or gustatory hallucinations, autonomic symptoms (change in BP, facial flushing), affective symptoms (fear, depersonalisation), deja vu
Seizure: motor arrest and absence, automatisms (lip smacking, chewing, fidgeting, walking), automatic speech, contralateral dystonia
Duration: slow evolution over 1-2 minutes
postictal: confusion, dysphasia
Frontal lobe seizures
Aura: typically abrupt onset with variable often indescribable aura, forced thinking or emotional manifests
Seizure: vocalisation, violent and bizarre automatisms, cycling legs, ictal posturing and tonic spasms, version of head and eyes contralateral to side of seizure focus, fencing posture (extending and abducting one arm with head rotation), sexual automatisms with pelvic thrusting, obscene gestures and genital manipulation
Duration: typically very brief around 30 seconds
Postictal: confusion brief with rapid recovery
Parietal lobe seizure
Somatosensory symptoms eg tingling, pain, prickling, vertigo, distortions or space
automatisms and secondary generalisation may occur
Occipital lobe seizures
Visual hallucinations - flashing lights, geometrical figures, sometimes complex hallucinations
eyelids might flutter, occasional eye turning or rapid blinking
automatisms and secondary generalisation might occur
Status epilepticus
If the seizure lasts >5 minutes
Is ongoing or without returning to normal
Usually caused by tonic clonic seizure but can occur from any type
Is a medical emergency - needs hospitalisation
Often treated with benzodiazepines to enhance GABA firing
Common after effects of seizures and investigations
After effects:
Postictal confusion
Paralysis (unilateral) of arms or legs Todd’s paralysis can last 15 mins subsides within 2 days. Thought to be caused by severe but temporary arrest from area of brain affected by seizure
Investigations:
MRI/CT brain
EEG electroencephalogram to detect electrical signals in brain
History to determine types; are they frequent, short, do they recall having them, third party info to describe features (absent, convulsions etc), any auras or symptoms before or after (postictal state), tongue biting and postictal confusion, urinary incontinence and pallor are NOT helpful as can occur with syncope. Any possible previous seizures
Full physical and neurological exam
Full mental state exam
Bloods: glucose, U+Es, Ca, eGFR, LFTs, urine biochemistry
Urgent neuro referral
Management of seizures
Specialist input within 2 weeks
EEGs to support diagnosis and MRI to identify structural abnormalities
Advice to cease driving, swimming or potentially dangerous work or leisure activities
Mainly anticonvulsants based on patients age and needs; usually not recommended until after second seizure, implemented once specialist diagnosis confirmed depending on risk of subsequent seizures occurring. Choice of drug based on type of seizure
Surgery to remove what is thought to be causing eg tumours of specific area of brain
Nerve stimulation
Ketogenic diet
Medication for seizures overview
Sodium valproate:
Increases GABA activity which relaxes the brain
Side effects: teratogenic (must be careful with contraception), liver damage and hepatitis, hair loss, tremor
Carbamazepine:
First line for focal seizure
Side effects: agranulocytosis, aplastic anaemia, induces the P450 system so has many drug interactions
Phenytoin:
Side effects: folate and vitamin D deficiency, megaloblastic anaemia (folate deficiency), osteomalacia (vit D deficiency)
Ethosuximide:
Side effects: night terrors and rashes
Lamotrigine:
Side effects: SJS or DRESS syndromes and leukopenia
Emergency management of seizures
Protect patient from injury, refrain from restraining, put cushioning under their head and clear area of dangerous objects
Don’t put anything in their mouth and TIME the seizures
When seizures stops: check airway, place in recovery position and check CV and neuro states
Prolonged seizures: (status epilepticus)
ABCDE approach:
Secure the airway
Give high-concentration oxygen
Assess cardiac and respiratory function
Check blood glucose levels
Gain intravenous access (insert a cannula)
IV lorazepam 4mg, repeated after 10 minutes if the seizure continues
If seizures persist: IV phenobarbital or phenytoin
Medical options in the community:
Buccal midazolam
Rectal diazepam
Pseudoseizures overview
Psychogenic nonepileptic seizures (PNES) occur as result of psychological cause such as severe mental stress rather than from neuronal dysfunction
Often result of other mental health conditions - treating underlying cause is vital
Aware of what’s happening and remember event
Response to touch unlike with actual seizure
Often have eyes closed unlike tonic clonic seizure so may also react to having eyes forced open
Show involuntary stiffening, convulsions and jerking, loss of attention, consciousness, confusion, absence or lack of awareness of surroundings
Conditions that may cause include: Generalised anxiety disorder Panic attacks OCD ADHD Substance abuse, traumatic injuries, emotional disturbance PTSD
In general, some treatments that may be effective for treating PNES include: (no prevention)
individual or family counseling
cognitive behavioral therapy (CBT)
relaxation techniques
behavioral therapy
eye movement desensitization and reprocessing (EMDR) therapy, for traumatic memories
antidepressants
medications for underlying psychological issues
general management principals
Headache diary: record frequency, duration and severity and monitor how well interventions are working
Give written and oral advice on medical disorder and information about support organisations
Warn of risks of medication overuse
Migraines
Complex neurological condition that causes headaches and other associated symptoms
Occurs in attacks often following a particular pattern
Most common cause of episodic headaches; affects up to 20% women and 10% men
Recognised cause of disability in those under age 50
May be a combination of structural, functional, chemical, vascular and inflammatory factors (thought the hypothalamus is involved especially in premonitory phase)
Types of migraines
Migraine without aura: characterised by headache with specific features and associated symptoms
Migraine with aura: primarily characterised by transient focal neurological symptoms before or during headache Silent migraine (with aura but without headache)
Hemiplegic migraine: aura includes motor weakness which can last for weeks, often have relatives with migraines with motor symptoms, gene mutations have been identified
Migraines with brainstem aura: dysarthria, vertigo, tinnitus, hearing impairment, diplopia, ataxia and decreased level of consciousness
Retinal migraines: repeated attacks of monocular visual disturbance - flashes of light (scintillations), scotomata, blindness
Chronic migraines: headaches occur on more than 14 days a month for more than 3 months. Migrainous headaches on at least 8 days a month. Check for medication overuse!!
Migraine without aura criteria
5+ headaches with typical characteristics of:
Unilateral pain
Pulsating
Moderate to severe intensity
Made worse by physical activity such as walking or climbing stairs
Associated with nausea or vomiting
Associated with photophobia and phonophobia
Lasting 4-72 hours
Normal examination and no other cause found
Migraines with aura
Around 25% migraine sufferers
Neurological symptoms immediately before or during headache
Some or all migraine attacks
Usually last for less than an hour (motor symptoms often lasting longer)
Usually precede headache
Neurological symptoms are fully reversible and may take several forms:
Visual - most common, shimmering, zigzags, fragmentation of image, patches of visual loss (scotomas, hemianopia and tunnel vision)
Sensory - tingling or pins and needles over part of the body, face or tongue. Numbness may follow or occur alone
Speech - dysphasia
Loss of motor function
Migraine triggers
Stress Hormones Alcohol Sleep change Bright lights Loud sounds Changes in weather Physical exertion
migraine presentation
Lasting between 4-72 hours Moderate to severe intensity Pounding or throbbing in nature Usually unilateral but can be bilateral Discomfort with lights - photophobia Discomfort with loud noises - phonophobia With or without aura Nausea and vomiting Severity varies between attacks and patients Frequently feel ‘washed out’ Hypersensitivity to touch
Hemiplegic migraine, presentation and triggers
Can mimic strokes
Essential to act fast and exclude stroke in patients presenting with these symptoms before considering hemiplegic migraine
Presentation: Typical migraine symptoms Sudden or gradual onset Hemiplegia (unilateral weakness of limbs) Ataxia Changes in consciousness
Triggers: often not possible to identify triggers Stress Bright lights Strong smells Certain foods Dehydration Menstruation Abnormal sleep patterns Trauma
5 stages of migraines and pathology
not typical in everyone and vary between patients, can experience only one or two stages. Prodromal stage can involve several days of subtle symptoms such as yawning, fatigue, food cravings, sore muscles or mood changes prior to onset of the migraine
Premonitory or prodromal stage - can begin 3 days before headache. Thought to be alternating body homeostasis (hypothalamic involvement).
Aura lasting up to 60 mins. Only 1/3rd patients experience this. Fully reversible neurological symptoms. Most common is visual: spotted or blurred vision, sensory aura, language aura or motor aura (weakness). Thought to be due to cortical spreading depression - neuronal depolarisation lasting longer than usual spreading across the cortex
Headache stage lasting 4-2 hours. Most commonly unilateral, pulsatile nature and may be accompanied by associated symptoms. Can experience changes in sensitivity to light, smell or touch (cutaneous allodynia).
Trigeminal vascular system thought to be activated by premonitory/aura phases causing trigeminal nerve to increase sensitivity in nociceptors in dura mater, referred pain then causing pain around the eye, occipital area etc due to conversion of nerves near the roots
Resolution stage - headache can fade away or be relieved completely by vomiting or sleeping
Post dromal or recovery phase. Lingering symptoms can be triggered by sneezing, moving etc. due to sensitisation in nociceptors in tissues which goes away in few days
acute management of migraines
Often go to dark room and sleep
Paracetamol 1g, high dose aspirin (900mg)
Triptans (sumatriptan 50mg as migraine starts; 5HT receptor agonists act on smooth muscle causing vasoconstriction, peripheral pain receptors inhibiting pain, reduce neuronal activity in CNS) try at least 3 migraines before moving on to alternative due to variability of effectiveness between patients must be taken at the start of headache phase (not useful in aura phase) CI in CVD, PVD, CVA or TIA. subcutaneous or nasal administration also available can repeat 50mg dose after 2 hours PRN but ONLY 2 doses <24 hours if migraines include vomiting then can give subcut injection (self administer)
NSAIDs - ibuprofen 400-600g or naproxen 250-500g
Antiemetics if vomiting occurs (metoclopramide 10mg, prochlorperazine 3-6mg buccal tablets)
Migraine prophylaxis
Avoiding known triggers; headache diary can help this
Physical activity as long as not a known migraine trigger and stop COCs in women whose migraines started or are worsened when taking them (increased cerebral thrombosis risk)
Propranolol 40mg BD-80mg up to 160mg - beta blocker first line
Anticonvulsants: Topiramate 25mg ON for 1 week then increase in 25mg steps to max 200mg - teratogenic and can cause cleft lip/palate so patients should not get pregnant
Amitriptyline 10mg increases 10mg weekly up to 60mg. Decreases neurotransmission. Side effects: can’t see, can’t pee, can’t spit, can’t shit
Sodium valproate initial 200mg BD up to 800mg
Botox for chronic migraines but inconsistent effectiveness
Acupuncture
Vitamin B12 supplements (riboflavin) may reduce frequency and severity
If migraine is specifically triggered around menstruation then prophylaxis with NSAIDs (mefenamic acid) or triptans (frovatriptan or zolmitriptan) can be used around that time as preventative measure
Can go into remission and tend to get better over time
Complications of migraines
Status migrainosus - debilitating attack lasting for than 72 hours
Persistent aura lasting over a week without evidence of infarction on imaging
Infarctions and seizures occurring during aura
GCA
Systemic immune related vasculitis affecting medium and large sized arteries, particularly carotid and its extracranial branches
Unknown pathogenesis but involves chronic inflammatory process, predominantly of large arteries
Highest incidences in northern EU countries
Most present 60-80 years
Cause is poorly understood: potentially autoimmune as often occurs in people with polymyalgia rheumatica
No well established triggers or risk factors
GCA presentation
Temporal headache and scalp tenderness Myalgia Malaise or fever Acute severe sight impairment (20% patients) Jaw claudication Diplopia Abnormal palpation of temporal artery - bruits may be heard over the carotid, axillary or brachial artery Elevated ESR Anaemia (normochromic normocytic anaemia) Features of polymyalgia rheumatica
GCA investigations and complications
Clinical
Temporal artery biopsy
Bloods: elevated ESR, CRP, LFTs (alkaline phosphatase can be elevated)
Colour duplex USS
complications
Loss of vision; permanent, partial or total
Aneurysms, dissections and stenotic lesions of aorta and major branches
CNS diseases: seizures, cerebral vascular accidents etc
Steroid related complications: osteoporosis, bruising, insomnia, hypomania, depression, HTN, diabetes, elevated cholesterol and fluid retention
GCA management
Fast Track referral to rheumatology (<3 days) for no ocular symptoms
Same day referral to ophthalmology if visual symptoms
40mg prednisolone daily
60mg prednisolone if claudication symptoms (jaw, tongue claudication or visual symptoms)
Once symptoms resolve can begin to reduce dose in 10mg steps biweekly, then in 2.5mg steps
Flares treated with increased corticosteroids to level at which symptoms were previously controlled
Low dose aspirin 75mg daily unless CI to decrease rate of visual loss and strokes
With high dose aspirin start PPI to decrease risk
Osteoporosis prophylaxis for long term steroid therapies
Subarachnoid haemorrhage, risk factors and association
Bleeding into the subarachnoid space where the CSF is located
Usually the result of a ruptured cerebral aneurysm
Very high mortality and morbidity
Accounts for 5% strokes
mean age of patient is 50 YO
Risk factors: HTN Smoking Excessive alcohol consumption Cocaine use Family history Black family origin Females Age 45-70
Associated with:
Sickle cell anaemia
Connective tissues disorders (Marfan syndrome, Ehlers-Danlos)
Neurofibromatosis
Autosomal dominant polycystic kidney disease
Subarachnoid haemorrhage presentation
Typical history is sudden onset occipital headache, occurs during strenuous activity. Known as the thunderclap headache due to suddenness and severity
Neck stiffness
Photophobia
Vision changes
Neurological symptoms such as speech changes, weakness, seizures and loss of consciousness
Subarachnoid haemorrhage investigations
CT head first line - blood causes hyperattenuation in the subarachnoid space
Lumbar puncture CSF analysis : RBC raised and xanthochromia (yellow colour caused by bilirubin)
Angiography (CT/MRI) once haemorrhage confirmed to locate source of bleed
Subarachnoid haemorrhage management
Referral to specialist neurosurgical unit
Reduced consciousness may need intubation and ventilation
Supportive care and MDT approach: nursing, nutrition, physio, occupational therapy
Surgical intervention to repair vessel and prevent rebleeding, can be done by coiling (inserting catheter into arterial system, placing platinum coils into aneurysm and sealing it off from artery) or clipping (cranial surgery clipping aneurysm to seal it)
Nimodipine is CCB used to prevent vasospasm. Vasospasm is a common complication that can result in brain ischaemia following haemorrhage
Lumbar puncture or inserting shunt to treat hydrocephalus
Antiepileptic medications to help seizures
Sinusitis
Causes headache with inflammation in ethmoidal, maxillary, frontal or sphenoid sinuses (PARANASAL SINUSES)
Acute: infection lasting 7-30 days. Tends to arise from viral infection with secondary bacterial infection. Commonly strep pneumoniae, H. influenzae
Subacute: infection lasting 4-12 weeks
Recurring: >3 significant acute episodes in a year lasting >10 days with no intervening symptoms
Chronic: symptoms persisting >90 days with or without acute exacerbations (can be caused by irreversible changes in mucosal lining of sinuses). Is multifactorial including infectious, inflammatory or structural
Sinusitis risk factors
Allergies Asthma Smoking Hormonal status (pregnancy etc) Nasal dryness Foreign body Irritant inhalation (cocaine) Dental problems - trauma or infection Swimming, divind, high altitude sports Mechanical obstruction (nasal polyps) Immunocompromised
Sinusitis presentations
This usually produces facial pain behind the nose, forehead and eyes
Often tenderness over affected sinus helping establish diagnosis
Usually resolves within 2-3 weeks
Most sinusitis is nasal. Nasal irrigation with saline can be helpful
Prolonged symptoms can be treated with steroid nasal spray, antibiotics sometimes needed
Acute cases present with non-resolving cold >1 week or worsening symptoms over 4-5 days. Initial viral infection rhinitis appears to settle followed by further malaise relating to the sinusitis
Headache
Cough
Dental pain
Pressure or fullness feeling in ears
Sinusitis investigations
History
Clinical diagnosis - palpate frontal (press up from beneath medial supraorbital ridge), maxillary (press against anterior wall below inferior orbital margin) and ethmoidal sinuses (press medially against medial wall of orbit) for tenderness
percussion and transillumination of sinuses
trigeminal neuralgia
Chronic debilitating condition resulting in intense and extreme episodes of facial pain
Episodes are sporadic and sudden often like electric shocks lasting several seconds to minutes
It is a result of neuropathic disorder of the 5th cranial nerve (trigeminal)
Trigeminal nerve supplies sensation, nociception, thermoception and motor supply to muscles of mastication
Most commonly the maxillary and/or mandibular branch are involved too
Uncommon in those younger than 40
May be genetic predisposition but exact transmission method is unclear
Triggers: Vibration Skin contact eg shaving or washing Brushing teeth Oral intake Exposure to wind
Trigeminal neuralgia presentation
Unilateral usually on the cheek or face but can involve the eyes, lips, nose and scalp
Sudden onset, brief duration
Stabbing, severe shock like pains
Recurrent pain occurring in paroxysms lasting from few seconds to minutes
May have preceding symptoms such as tingling or numbness
Can have triggers
Episodes are intermittent but can last days, weeks, months on end then not return for months or years etc.
Atypical presentations have restless underlying pain like a migraine associated with superimposed stabbing pains and maybe intense burning sensation. This is more difficult to treat
Red flags trigeminal neuralgia
Sensory changes, deafness or other ear problems
Difficulty achieving pain control, poor response to carbamazepine
History of skin lesions or oral lesions that could lead to perineural spread
Ophthalmic division only or bilateral suggestive of malignant lesions or MS
Age onset under 40 years
Optic neuritis
Family history of MS
trigeminal neuralgia investigations and complications and prognosis
Clinical diagnosis
MRI for uncertainty
Complications:
Poor quality of life due to severe pain
Poor mental and physical capacity
Prognosis:
50% experience remissions of at least 6 months duration
65% newly diagnosed will have second episode within 5 years
Periods of remission tend to get shorter with time and attacks of pain tend to get longer
Trigeminal neuralgia management
No definitive cure at present, but newer surgical procedures are promising
Offer carbamazepine first line
If ineffective or severe pain limiting daily activities or atypical clinical features consider expert advice or early referral to specialist pain service
Reassure patient it is not life threatening, education on condition and management options, avoiding triggers, support groups etc
Gabapentin combined with ropivacaine injections into trigger sites can improve pain control
Botox injection to reduced frequency and pain intensity
Surgery - relieving pressure on nerve (microvascular decompression) or damaging it to prevent pain transmission (Rhizotomy)
Chronic pain commonly impacts and risk factors:
Difficulty sleeping most commonly Lack of energy Drowsiness Concentration difficulties Depression Anxiety Poor appetite Can lead to mental health problems - anxiety, depression etc
Risk factors:
Older age
Female
Lower income and social deprivation
Geographical and cultural background: South asian more common
History of abuse or interpersonal violence
Employment and occupation: heavy lifting etc.
Classifications of pain
Acute (<3 months)
Chronic (>3 months, or beyond expected healing time)
Underlying mechanism - nociceptive (ability to detect painful stimulus, protects against injury) vs neuropathic (arising from nerve damage, serves no protective purpose)
Physical origin - visceral (organs) vs somatic (external body- soft tissues, bones, muscles) referred pain
Underlying cause - cancers, inflammatory (often worse at night or early day), post-operative (predictable likely acute nociceptive), mechanical pain (related to movements)
Acute and chronic pain pathology
Acute: Usually resolves in less than 3 months Burns Broken bones Sprained joints Acute pain is commonly nociceptive but can be neuropathic (eg herpes zoster virus)
Chronic:
Acute pain can sometimes persist becoming chronic; this is because repeated exposure to painful stimuli can cause alterations in the nervous system making them more sensitive to painful stimuli. For example, inflammation associated with pain can cause peripheral sensitisation which increases pain intensity and the area the pain is felt. Repeated painful stimuli causes a ‘wind up’ leading to more intense pain felt and more pain signals transmitted leading to central sensitisation leading to people feeling pain when they should not eg those with severe cases can feel pain with touch
Chronic mechanical pain is nociceptive pain
Nociceptive vs neuropathic pain
Nociceptive pain:
Typically sharp pain or dull ache
Degree of pain usually proportional to cause
Can easily describe pain usually
Likely to respond to simple analgesic (NSAID, paracetamol, opioids)
Neuropathic pain:
Often difficult to describe
Burning, shooting, crawling, electric shocks, stabbing pains
May appear out of proportion to cause
Likely to best respond to antineuropathic medications (tricyclic antidepressants like amitriptyline, gabapentinoids like pregabalin or gabapentin)
Pain pathways
Several pathways transmit pain signals
Most importantly the spinothalamic tract which transmits touch and temperature
Other pathways: spinoreticular tract and spinomesencephalic tract
Pain signals pass from periphery to spinal cord then to midbrain, then travels out to several other areas (ascending pathway)
Brain influences pain perception via descending pathway blocking ascending transmission. Descending pathway NTs include endorphins (natural opioids), NA and serotonin. Effectiveness of descending pathway varies with situation and brain state eg when in state of threat/danger may not feel pain until conflict is resolved, but person with low mood may feel pain more than normally expected from injury
Spinothalamic:
Consists of medial and lateral tracts
Lateral carries sensory discriminative part of signal and enables sufferer to localise pain
Medical tract terminates deeper in brain causing general arousal and aversion
Spinoreticular tracts:
Terminated in reticular formation of medulla and pons contributes to general arousal associated with pain
Spinomesencephalic:
Synapses in area of midbrain called periaqueductal grey
Stimulation causes release of endogenous opioids inhibiting pain signals in spinal cord causing natural analgesia
Pain red flags
Possible fractures
Major trauma
Minor trauma in elderly or degenerative bone diseases
Age <20 or >50
History of cancer
Weight loss
Recent bacterial infection
Previous IV drug use
Immunosuppression
Severe worsening pain, especially at night or lying supine
Severe or progressive sensory alteration or weakness
Bladder or bowel dysfunction
Evidence of neurological deficit on physical exam
Visual disturbance
Unexplained seizures
Pain yellow flags
flags indicating increased likelihood of developing chronic pain:
Anxiety
Beliefs that pain is always harmful and activity can cause more damage
Catastrophizing
Depression
Expectation that only passive treatments will help and reluctance to be involved in active participation
Fear avoidance behaviour
Severe pain intensity
Adopting ‘illness’ type behaviours
Mood disruption, avoidance of social contact
Requesting treatment that does not fit best practice or is against clinical judgement
Ongoing litigation
Social and financial problems
History of extended sick leave or other absence
Problems at work or poor job satisfaction
Overprotective family or lack of support
Signs of neuropathic pain
Allodynia, by gently stroking the affected area with a brush, cotton wool or a feather, which causes an exaggerated pain response from the patient
Hyperalgesia, by a normal painful stimulus using a pin, which causes a greatly increased pain response from the patient
Quantifying pain
various assessment scales and questionnaires, such as: Visual analogue scale (VAS) Numerical rating scale (NRS) Verbal rating scale (VRS) Visual signs of pain Physical signs
Pain assessment tools are divided into the following three types:
Unidimensional scales (mainly used for acute pain)
Multidimensional scales
Diagnostic questionnaires The Leeds assessment of neuropathic symptoms and signs (LANSS)
The Douleur Neuropathique 4 (DN4)
PainDETECT
conditions to be aware of if taking NSAIDs
Asthma (may worsen)
Renal impairment increased risk of dehydration
Liver impairment cautioned in liver disease
Upper GI bleeding or ulceration
HF or previous heart attack - increased risk of this and stroke
Pregnant
Opioid overview
acts on multiple opioid receptors in the body (distributed throughout nervous system (CNS and PNS). OP3 thought to mediate most analgesic properties. Activate receptor and signalling pathways reducing transmission of nociceptive impulses
Codeine is an opioid PROdrug meaning needs to be converted to active form in liver, as is tramadol, dihydrocodeine and oxycodone
drug interactions: alcohol enhance drowsiness, SSRIs increase risk of serotonin syndrome
IV morphine should only be given in a place where oxygen and resuscitation facilities are available. Patient observations including the respiratory rate should be monitored until at least 15 minutes after the last dose.
Morphine requires an effective renal system to clear its metabolites. Patients suffering from renal failure may require a reduction in the dose of the drug.
Naloxone can be used for opioid overdose antidote
PCA
Patient-controlled analgesia (PCA) enables a patient to control a pump, on demand, to administer small bolus doses of analgesic drugs. The most common drug used is morphine, but other analgesic agents, such as fentanyl, oxycodone and ketamine, are also used.
Safety features of a PCA pump include:
Limited size of bolus
Lockout interval
Limited total dose administered
Most hospitals have a PCA protocol. A typical adult PCA protocol administers 1 mg of morphine with a 5 minute lockout.
In children, and patients who are not able to use PCA, the responsibility is given to the nurse looking after the patient. This is called nurse‑controlled analgesia (NCA). It is important that only the nurse administers a dose. The pump usually has a longer lockout period to prevent serious adverse side-effects.
If the patient is still requiring the PCA after a few days and is able to eat and drink, it may be appropriate to change the PCA to oral medication.
Opioid common side effects
constricted pupils
drowsiness, confusion and hallucinations
respiratory depression
reduced HR and low BP, palpitations and oedema
anaemia and low platelets
nausea, vomiting and constipation
bone mineral density decreased, joint pain and weakness
urinary retention
skin itching
Opioid drugs doses and equivalent dose to oral morphine
Codeine - 60mg - 3-9mg equivalent
tramadol - 100mg - 10mg equivalent
morphine IV/IM 10mg - 20-40mg equivalent
fentanyl - 100micrograms - 10mg
Neuropathic pain management
Gabapentin - effective and also enhances analgesic effect of morphine if given alongside.
Pregabalin - second line produces similar effects. both stimulates production and release of GABA
side effects: dizziness, headache, tremor, nausea and vomiting, diplopia, nystagmus, ataxia, oedema and drowsiness
Antidepressants - amitripylline (tricyclic) at LOW doses is effective analgesic and evidence to suggest it reduced chronic herpes zoster pain
BEST TAKEN 60-90 minutes before bed (less hangover effect) and increase in slow increments if experiencing bad side effects
Duloxetine is an SNRI been shown to reduce pain of diabetic neuropathy
opioids can be helpful (tramadol and oxycodone)
Linodcane patches and capsaicin creams useful for post herpetic neuralgia
Simple analgesics along with non-pharmacological therapies - TENS
Non-pharmacological pain relief methods
Neuromodulation is considered for certain kinds of pain:
- acupuncture: effective for peripheral joint osteoarthritis and can be appropriate to try 6 week course in most types of pain
- TENS has no evidence of benefit despite many women claiming it helps in during labour
- spinal cord stimulators SCSs: shown to help failed back surgery syndrome and complex regional pain syndrome, also recommended for chronic neuropathic pain
other methods:
- CBT for effective pain management techniques in chronic pain
- structured exercise program eg physiotherapy recommended for lower back pain
- radiation therapy very effective at palliating symptoms for bony metastases along with surgical neuroablative techniques
Common pain relief drugs method of action
Ibuprofen - inhibits cycloxygenase
Morphine - acts on cell membrane opioid receptors
ketamine - blocks NMDA receptors
Gabapentin - stimulates GABA production
How to discuss medications with patients BRAN
benefits of treatment,
Risks,
Alternatives,
Nothing - what might happen if the patient does nothing
Subarachnoid haemorrhage complications and prognosis
Complications:
Rebleeding (most common cause of death; 20% in first few days)
Vasospasm causing cerebral ischaemia - most common cause of permanent CNS deficit (peaks at days 4-12)
Hydrocephalus (first 24 hours) due to blockage of arachnoid granulations needing ventricular or lumbar drainage
SIADH causing hyponatremia
Prognosis:
Not good; 50% die suddenly soon after bleeding
10-20% die in early weeks in hospital from rebleeding
May have long term FND
Subarachnoid haemorrhage pathology
Rupture (70% Berry aneurysms) mainly branching points of circle of willis
10% congenital arteriovenous malformations
20% no lesions found
Main cerebral arteries in circle of willis common for berry aneurysms are:
anterior communicating artery
origin of posterior communicating artery
trifurcation of middle cerebral artery
termination of internal carotid artery
basilar artery
Subarachnoid haemorrhage complications and prognosis
Complications:
Rebleeding (most common cause of death; 20% in first few days)
Vasospasm causing cerebral ischaemia - most common cause of permanent CNS deficit (peaks at days 4-12)
Hydrocephalus (first 24 hours) due to blockage of arachnoid granulations needing ventricular or lumbar drainage
SIADH causing hyponatremia
Prognosis:
Not good; 50% die suddenly soon after bleeding
10-20% die in early weeks in hospital from rebleeding
May have long term FND
Subarachnoid haemorrhage pathology
Rupture (70% Berry aneurysms) mainly branching points of circle of willis
10% congenital arteriovenous malformations
20% no lesions found
Main cerebral arteries in circle of willis common for berry aneurysms are:
anterior communicating artery
origin of posterior communicating artery
trifurcation of middle cerebral artery
termination of internal carotid artery
basilar artery
Raised ICP
Syndrome, often a complication rather than stand alone presentation
Can be acute (trauma) or chronic (eg SOL: brain tumour, abscess, haematoma)
Pathophysiology:
Skull is incompressible and volume inside is fixed
80% volume brain; 10% blood and 10% CSF
Therefore if one component increases then the other must decrease to compensate eg hematoma increases blood so CSF may be diverted down into spinal column
If these changes are too much for compensatory mechanisms then this leads to increased ICP
Cerebral perfusion pressure = MABP - ICP
Main mechanisms:
Oedema caused by stroke, CVA, trauma, hyponatremia
SOL caused by brain tumours, brain abscess, ICH
CSF or venous system blockage caused by hydrocephalus, CVT/IVT etc
