Neuro + gerries Flashcards

1
Q

What are the four different types of dementia?

A
  • Alzheimers
  • Vascular
  • Lewy Body
  • Frontotemporal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the cause of Alzheimer’s disease?

A

Unknown cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the pathophysiology of Alzheimer’s Disease?

A

Neurofibrillary tangles
beta-amyloid protein accumulations - beta-amyloid plaque
Neurodegenerative disease - neuronal damage
Decreased Ach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the risk factors for Alzheimer’s disease?

A

–> Downs syndrome
–> Amyloid precursor protein gene mutation
–> older age
–> 1st degree relative, FHx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the signs and symptoms of Alzheimer’s disease?

A

–> progressive global cognitive impairment
–> aphasia
–> Anosognosia - unaware of their own illness
–> Short-term memory loss which is progressive and persistent
–> irritable
–> mood swings
–> apathy - lack of interest/motivation
–> behavioural changes –> confusion, wandering, aggression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the investigations for Alzheimer’s disease?

A

–> CT to look for brain atrophy
–> MMSE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What medication can be given for Alzheimer’s disease?

A

–> Acetylcholinesterase inhibitors –> Donepezil, Rivastigmine
–> memantine –> glutamate receptor antagonist
–> NMDA receptor antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the pathophysiology of vascular dementia?

A

The cumulative effect of many small strokes/TIA’s, stepwise
Grey and white matter damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the risk factors for vascular dementia?

A

–> HTN
–> DM
–> age
–> hyperlipidaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the symptoms of vascular dementia?

A

–> Sudden Onset
–>Stepwise deterioration
–>motor disorders
–> behavioural changes
–> cog impairment
–> Depressions/labile mood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the investigations for vascular dementia?

A

–> MMSE
–> Carotid USS
–> CT/MRI head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the treatment for vascular dementia?

A

–> Treat the risk factors –> antiplatelets, aspirin (secondary prevention)
–> Cholinesterase inhibitors if AD comorbidity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the pathophysiology of Parkinson’s disease?

A

progressive reduction of dopamine from the substantia nigra in the basal ganglia leading to movement disorders.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the symptoms of Parkinson’s disease?

A

–> Characteristically asymmetrical with one side affected more than the other
–> Classic triad –> Resting tremor - pill-rolling tremor more pronounced on voluntary movement or distracted/ cogwheel rigidity - tension in their arm that gives way to move in small increments (like little jerks). / bradykinesia - movements getting slower and smaller - handwriting getting smaller, shuffling gait, difficulty initiating movement, difficulty turning around, reduced facial movement or expressions (hypomimia)
–> postural instability
–> stooped posture
–> facial masking - reduced facial expressions
–> forward tilt
–> reduced arm swing
–> shuffling gait
–> depression
–> sleep disturbance
–> cognitive impairment and memory issues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How can you distinguish between the tremor of Parkinson’s disease and benign essential tremor?

A

Parkinson’s Tremor
–> Asymmetrical
–> 4-6 Hertz
–> worse at rest
–> improves with intentional movement
–> other Parkinson’s features
–> no change with alcohol
Benign essential tremor
–> Symmetrical
–> 5-8 Hertz
–> improves with rest
–> Worse with intentional movement
–> No other Parkinson’s features
–> improves with alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are Parkinson’s plus syndromes?

A

a group of neurodegenerative diseases featuring the classical features of Parkinson’s disease (tremor, rigidity, akinesia/bradykinesia, and postural instability) with additional features that distinguish them from simple idiopathic Parkinson’s disease

–> Multiple system atrophy –> Neurones of multiple systems in the brain degenerate, affecting the basal ganglia as well as other areas, degeneration of basal ganglia leads to Parkinson’s symptoms and degeneration in other areas leads to autonomic dysfunction e.g postural hypotension, constipation, abnormal sweating and sexual dysfunction and cerebellar dysfunction - ataxia
–> dementia with Lewy bodies - This is a type of dementia associated with features of Parkinsonism. It causes a progressive cognitive decline. There are associated symptoms of visual hallucinations, delusions, disorders of REM sleep and fluctuating consciousness.
–> progressive supranuclear palsy –> A tauopathy: neurofibrillary tangles of tau protein Parkinsonism + postural instability and falls, + vertical gaze palsy, + symmetrical onset, + truncal rigidity
–> Corticobasal degeneration –> A tauopathy: neurofibrillary tangles of tau protein Parkinsonism + apraxia,+ aphasia ,+ asterognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How would you diagnose Parkinson’s disease?

A

–> Clinically based on symptoms and examination
–> UK Parkinson’s disease society brain bank clinical diagnostic criteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the management of Parkinson’s disease?

A

–> Levodopa - synthetic dopamine - less effective over time
–> Peripheral decarboxylase inhibitors - stops dopamine breaking down before it reaches the brain - Carbidopa/Benserazide
–> COMT inhibitors - entacapone - slows the breakdown of levodopa in the brain
–> Dopamine agonists - mimic dopamine in the basal ganglia and stimulate the dopamine receptors - less effective compared to levodopa but can delay the use of levodopa - cabergoline/pergolide/ bromocryptine
–> Monoamine Oxidase-B inhibitors –> Monoamine oxidase enzymes break down neurotransmitters such as dopamine, serotonin and adrenaline. The monoamine oxidase-B enzyme is more specific to dopamine and does not act on serotonin or adrenalin. These medications block this enzyme and therefore help increase the circulating dopamine - selegiline/ rasagiline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is benign essential tremor

A

–> most common movement disorder associated with older age
–> fine tremor affecting all voluntary muscles
–> most notable in the hands but can affect head, jaw and vocal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the features of a benign essential tremor?

A

–> Fine tremor
–> Symmetrical
–> More prominent on voluntary movement
–> Worse when tired, stressed or after caffeine
–> Improved by alcohol
–> Absent during sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the differential diagnoses of tremors?

A

–> Parkinson’s disease
–> Multiple sclerosis
–> Huntington’s Chorea
–> Hyperthyroidism
–> Fever
–> Medications (e.g. antipsychotics)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the management of a benign essential tremor?

A

–> no definitive treatment, medication can improve symptoms
–> propranolol - non-selective beta-blockers
–> Primidone - anti-epileptic medication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is motor-neurone disease?

A

–> umbrella term for a variety of specific diagnoses
–> progressive and ultimately fatal where the motor neurones stop functioning
–> no effect on the sensory neurones
–> progressive degeneration of the upper and lower motor neurones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the different types of motor neurone disease?

A

–> amyotrophic lateral sclerosis (ALS) - most common
–> progressive bulbar palsy
–> progressive muscular atrophy
–> primary lateral sclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is amyotrophic lateral sclerosis and what is the presentation?
--> most common motor neurone disase --> progressive spasticity --> weakness and wasting with added lower motor neurone signs --> fasciculations --> UMN+ LMN
26
What is progressive bulbar palsy and what is the presentation?
--> second most common motor neurone disease --> Bulbar describes LMN signs from the 9th, 10th and 12th cranial nerve lesions --> wasted fibrillating tongue/ flaccid tongue --> commonly affects the muscles involved in swallowing and talking --> dysarthria --> dysphagia --> regurgitation and choking on fluids --> eye movements are unaffected --> UMN+LMN
27
What is progressive muscular atrophy and what is the presentation?
--> type of motor neurone disease --> LMN only --> wasting begins in the small muscles of the hand --> fasciculations is common --> cramps occur --> anterior horn cells affected --> distal muscles are affected first then proximal
28
What is primary lateral sclerosis and what is the presentation?
--> rare type of motor neurone disease --> Progressive tetraparesis (muscular weakness affecting all four extremities) --> UMN affected only
29
What are the risk factors and potential causes of motor neurone disease?
--> 5-10% of inherited cases --> increased risk with smoking, exposure to heavy metals and certain pesticides
30
What are the signs of lower motor neurone disease?
--> muscle wasting --> reduced tone --> fasciculations --> reduced reflexes
31
What are the signs of Upper motor neurone disease?
--> increased tone or spasticity --> brisk reflexes --> upgoing plantar responses --> clonus - involuntary muscle contractions
32
How is motor neurone disease diagnosed?
--> clinical presentation and excluding other conditions
33
What is the management of motor neurone disease?
--> no definitive treatment --> Riluzole can slow the progression of the disease --> MDT --> end of life care --> non-invasive ventilation can be used to support breathing at night
34
What is multiple sclerosis/ pathophysiology?
--> Chronic and progressive condition --> demyelination in the CNS (Oligodendrocytes) --> inflammatory process involving the activation of immune cells (T cells) against the myelin --> lesions of demyelination vary in their location over time --> disseminated in time and space
35
What are the potential causes of multiple sclerosis?
--> cause is unclear, could be caused by: --> Multiple genes -->Epstein–Barr virus (EBV) --> Low vitamin D --> Smoking --> Obesity
36
In who does Multiple sclerosis typically present in?
Women under 50
37
What are the signs and symptoms of multiple sclerosis?
--> optic neuritis - most common presentation - demyelination and loss of vision in one eye - decreased visual acuity, pain on eye movement, dyschromatopsia , central scotoma - enlarged blind spot --> sensory - trigeminal neuralgia/numbness/paresthesia/ Lhermitte's sign --> motor - transverse myelitis, UMN weakness, uhtoff's phenomenon - worsening of symptoms when the body is overheated/ limb paralysis/ bells palsy/ horners syndrome --> other - Ataxia is problems with coordinated movements that can be sensory (loss of proprioception) or cerebellar/ erectile dysfunction/ urinary incontinence
38
What are the different disease patterns of Multiple sclerosis?
--> Clinically isolated syndrome - first episode of demyelination and signs, cannot be diagnosed as the lesions are not disseminated in time and space --> Relapsing-remitting - most common - episodes of disease followed by recovery, In MS the symptoms occur in different areas with different episodes --> Secondary progressive - Secondary progressive MS is where there was relapsing-remitting disease at first, but now there is a progressive worsening of symptoms with incomplete remissions. Symptoms become more and more permanent --> Primary progressive - Primary progressive MS is where there is a worsening of the disease and neurological symptoms from the point of diagnosis without initial relapses and remissions
39
How are the diagnoses made for multiple sclerosis?
--> Diagnosis is made by a neurologist based on the clinical picture and symptoms suggesting lesions that change location over time. Symptoms have to be progressive over a period of 1 year to diagnose primary progressive MS. Other causes for the symptoms need to be excluded. --> MRI scans to look for lesions --> Lumbar puncture to look for oligoclonal bands in CSF
40
What are other causes of optic neuritis?
Sarcoidosis Systemic lupus erythematosus Diabetes Syphilis Measles Mumps Lyme disease
41
What is the management of multiple sclerosis?
Acute relapses: Methylprednisolone oral/IV chronic: disease-modifying drugs and biologics - Interferon/Glatiramer, Natalizumab
42
What is muscular dystrophy?
an umbrella term for genetic conditions that cause gradual weakening and wasting of muscles
43
What is the main muscular dystrophy to be aware of?
Duchenne muscular dystrophy
44
Give examples of different muscular dystrophies
Duchennes muscular dystrophy Beckers muscular dystrophy Myotonic dystrophy
45
What sign would you see in a child with Duchenne muscular dystrophy?
Gower's sign - child uses their hands on their legs to help them stand up due to proximal muscle weakness
46
What is the underlying genetic inheritance of Duchenne's muscular dystrophy?
X-linked recessive - males more common
47
What is Duchenne's Muscular dystrophy?
An X-linked (males more common) recessive disorder characterised by progressive muscle wasting and weakness
48
What is the pathophysiology of Duchenne's muscular dystrophy?
--> Damage to the dystrophin gene --> no dystrophin produced --> dystrophin is used to strengthen and protect muscle fibres from injury
49
What is the prognosis of Duchenne's muscular dystrophy?
--> wheelchair by 12 and death by 30
50
What are the signs and symptoms of Duchenne's muscular dystrophy?
Present in early childhood, before 3 ● Progressive proximal muscular dystrophy with characteristic pseudohypertrophy of the calves ● Major milestones delayed ● Inability to run, hop or jump ● Recurrent falls ● Speech delay ● Fatigue - really common
51
What are the investigations for Duchenne's muscular dystrophy?
Initial investigation - serum creatinine kinase Very high ● Genetic analysis ● Muscle biopsy with an assay for dystrophin protein ● Muscle strength test ● Gait assessment
52
What are the complications of Duchenne's muscular dystrophy?
Joint contractures ● Respiratory failure - most common cause of death ● Cardiomyopathies and heart failure ● Gastric dilation ● Learning difficulties ● Constipation, osteoporosis, hypertension
53
What is the management for Duchenne's muscular dystrophy?
MDT care ● Specialist referral ● Immunisations - influenza and pneumococcal ● Physiotherapy ● Vitamin D and bisphosphonates for bone health ● Corticosteroids ● Mobility help - wheelchair once cannot walk ● Nutritional care ● End-of-life directive and palliative set-up
54
What is Becker's muscular dystrophy?
--> Similar to Duchenne's --> dystrophin gene less affected/maintains some of its function --> symptoms appear later around 8, some can walk assisted in adulthood --> similar management to Duchenne's
55
What are the typical features of myotonic dystrophy?
Progressive muscle weakness Prolonged muscle contractions - e.g not being able to let go of someones hand after shaking Cataracts Cardiac arrhythmias
56
What is Huntington's disease?
autosomal dominant progressive neurodegenerative disease 100% penetrance - all who carry the gene express the trait trinucleotide repeat disorder
57
What is the pathophysiology of Huntington's disease?
Associated with cell loss within the basal ganglia and cortex ● Essentially too much dopamine ● See an increase in CAG repeats on the Huntington gene, on chromosome 4p16.3
58
Who does Huntington's disease affect the most?
Male aged 30-50
59
Huntington's disease displays genetic anticipation, what is anticipation?
Where successive generations have more trinucleotide repeats in the gene which results in --> earlier age of onset --> increased severity of the disease
60
What is the presentation of Huntington's disease?
It typically begins with cognitive, psychiatric or mood problems, followed by the development of movement disorders: Chorea (involuntary, random, irregular and abnormal body movements) Dystonia (abnormal muscle tone, leading to abnormal postures) Rigidity (increased resistance to the passive movement of a joint) Eye movement disorders Dysarthria (speech difficulties) Dysphagia (swallowing difficulties)
61
What are the investigations for Huntington's disease?
● MRI/CT - loss of striatal volume ● Genetic testing ● Tests for SLE, thyroid disease, Wilson’s disease and dementia
62
What is the management of Huntington's disease?
Management only, drugs do not affect on progression of condition ● Benzodiazepines (Diazapam) /valproic acid - chorea ● SSRIs if depression present ● Haloperidol for psychosis ● Prognosis is poor ○ Most common death is from concurrent illness, e.g. pneumonia ○ Suicide is the 2nd most common cause
63
What is meningitis?
--> inflammation of the meninges --> inflammation usually due to bacterial or viral infection
64
What are the causes of meningitis in Neonates, children, adults and the elderly?
Neonates: GBS - Group B strep, E-coli Children: Haemophilus influenza, Neisseria meningitides, strep pneumoniae (pneumococcus) Adults: Neisseria meningitides (meningococcus), Strep pneumonia Elderly: Strep pneumoniae
65
What type of bacteria is Neisseria meningitidis?
gram-negative diplococcus also known as meningococcus
66
What is meningococcal septicaemia?
--> meningococcus (Neisseria meningitides) bacterial infection in the bloodstream. --> Meningococcal refers to the bacteria and septicaemia refers to an infection in the bloodstream. --> cause of the classic “non-blanching rash”. This rash indicates the infection has caused disseminated intravascular coagulopathy (DIC) and subcutaneous haemorrhages.
67
what is Meningococcal meningitis?
bacteria is infecting the meninges and the cerebrospinal fluid around the brain and spinal cord.
68
What is the presentation of meningitis?
--> Triad: Headache, neck stiffness, fever --> Acute bacterial infection: - Sudden onset - Papilloedema - usually bilateral - Systemic symptoms - Intense malaise, rigours, photophobia, - - vomiting - Reduced GCS, focal CNS signs, seizures Viral: Self-limiting lasting 4-10 days May have headaches for months afterwards Chronic: TB A long history of vague symptoms of headache, anorexia, and vomiting. Triad is absent or late sign --> if meningococcal septicaemia children can present with a non-blanching rash --> Neonates and babies can present with non-specific signs and symptoms, such as hypotonia, poor feeding, lethargy, hypothermia and a bulging fontanelle.
69
What are the two special tests that you can perform to look for meningitis?
Kernig’s test Brudzinski’s test
70
What is Kernig's test?
involves lying the patient on their back, flexing one hip and knee to 90 degrees and then slowly straightening the knee whilst keeping the hip flexed at 90 degrees. This creates a slight stretch in the meninges. Where there is meningitis it will produce spinal pain or resistance to movement.
71
What is Brudzinski's test?
involves lying the patient flat on their back and gently using your hands to lift their head and neck off the bed and flex their chin to their chest. A positive test is when this causes the patient to involuntarily flex their hips and knees.
72
What are the investigations for suspected meningitis?
LP: Bacterial: high protein, low glucose, high neutrophils Viral: normal protein, normal glucose, high lymphocytes TB: high protein, low glucose, high lymphocytes --> blood culture --> throat swabs - bacterial and viral
73
What are the NICE criteria for meningitidis investigations for all children?
Under 1 month presenting with fever 1 – 3 months with fever and are unwell Under 1 year with unexplained fever and other features of serious illness
74
What is the management of meningitis?
Community: Immediate IM or IV Benzylpenicillin Withhold treatment if true penicillin anaphylaxis, priority is transfer. Hospital: Ideally blood cultures and LP should be done, but do not delay treatment if acutely unwell. IV Cefotaxime or IV Ceftriaxone. Add IV Vancomycin in recent travellers Add amoxicillin in neonates and elderly ○ With rash - Benzylpenicillin IV (meningococcal septicaemia) ○ Without rash - Cefotaxime IV Prophylaxis: Contact in the last 7 days. A single dose of Oral Ciprofloxacin or Rifampicin (except in pregnancy). Corticosteroids - Oral dexamethasone to reduce cerebral oedema and complications (hearing loss, neurological damage). 4 times daily for 4 days to children over 3 months. Viral meningitis - LP can be done, usually self-limiting. Acyclovir may be used in HSV meningitis.
75
How does the appearance of CSF in bacterial and viral meningitis differ?
Bacterial - cloudy Viral - clear
76
What are the potential complications of meningitis?
Hearing loss, Seizures/epilepsy Cognitive impairment/disability Memory loss, Focal neurological deficit.
77
What is Guillian-Barre syndrome?
--> Guillain-Barré syndrome is an “acute paralytic polyneuropathy” that affects the peripheral nervous system - demyelination. --> It causes acute, symmetrical, ascending weakness and can also cause sensory symptoms. --> It is usually triggered by an infection and is particularly associated with campylobacter jejuni, cytomegalovirus and Epstein-Barr virus.
78
What is Guillian- Barre syndrome normally triggered by?
--> It is usually triggered by an infection and is particularly associated with campylobacter jejuni, cytomegalovirus and Epstein-Barr virus --> Commonly present post-GI infection (~6 weeks after)
79
What is the pathophysiology of Guillian- Barre syndrome?
Guillain-Barré is thought to occur due to a process called molecular mimicry. The B cells of the immune system create antibodies against the antigens on the pathogen that causes the preceding infection. These antibodies also match proteins on the nerve cells. They may target proteins on the myelin sheath of the motor nerve cell or the nerve axon.
80
What is the presentation of Guillian-Barre syndrome?
--> Symmetrical ascending weakness (starting at the feet and moving up the body) - TOE TO NOSE WEAKNESS --> hyporeflexia (LMN sign) --> There may be peripheral loss of sensation or neuropathic pain or paraesthesia --> It may progress to the cranial nerves and cause facial nerve weakness --> Involvement of the autonomic nervous system ○ Reduced sweating ○ Reduced heat tolerance ○ Paralytic ileus - intestinal obstruction w/o blockage ○ Urinary hesitancy
81
What is the clinical course of Guillian-Barre syndrome?
Symptoms usually start within 4 weeks of the preceding infection. The symptoms typically start in the feet and progress upward. Symptoms peak within 2-4 weeks, then there is a recovery period that can last months to years.
82
How is a diagnosis of Guillian-Barre syndrome made?
--> clinical diangosis --> Brighton criteria --> nerve conduction studies - reduced signal through nerves --> Lumbar puncture - Raised protein with a normal cell count and glucose
83
What is the management for Guillian- Barre syndrome?
--> IV immunoglobulins --> Plasma exchange (alternative to IV IG) --> Supportive care --> VTE prophylaxis (pulmonary embolism is a leading cause of death) e.g LMWH --> avoid corticosteroids as can make symptoms worse --> good prognosis, most recover
84
What is encephalitis?
Infection and inflammation of the brain parenchyma. Broad term with various causative agents. Most commonly caused by viruses.
85
What are the causes of encephalitis?
Viral - most common HSV VZV, EBV, CMV, HIV, measles, mumps, arboviruses (West Nile) Non-viral - Bacteria, fungal, parasitic TB, Mycoplasma, Rickettsia, Bacterial meningitis (Listeria, Neisseria) Cryptococcus, Histoplasmosis Malaria, Toxoplasmosis, Schistosomiasis Non-infectious - Paraneoplastic Post-infectious Autoimmune
86
What is the pathophysiology of encephalitis?
An intracranial infection provokes an inflammatory response causing inflammation of the cortex, white matter, basal ganglia and brain stem depending on the causative organism. This results in neurological signs and systemic signs of infection. The frontal and temporal lobes are mostly affected. `
87
What is the presentation of encephalitis?
Classic triad - Fever, headache, altered mental status/focal neurological signs: Insidious onset, can also be abrupt - Features of a viral infection to begin with - fever, malaise, nausea, headaches - Behavioural change - a common early sign - Decreased consciousness, confusion - Focal neuro signs - cranial nerve palsies, hemiparesis, cerebellar ataxia, dysphagia, dysarthria - Seizures - Signs of raised ICP may lead to coma
88
What are the differentials of encephalitis?
Anything that causes behavioural change DKA Hypoglycaemia Hepatic encephalopathy B1 (thiamine) deficiency also called Beri-beri Meningitis Stroke Drug overdose Brain tumour
89
What are the investigations for encephalitis?
--> Lumbar puncture, sending cerebrospinal fluid for viral PCR testing --> CT scan if a lumbar puncture is contraindicated --> MRI scan after the lumbar puncture to visualise the brain in detail --> EEG recording can be helpful in mild or ambiguous symptoms but is not always routinely required --> Swabs of other areas can help establish the causative organism, such as throat and vesicle swabs --> HIV testing is recommended in all patients with encephalitis --> Contraindications to a lumbar puncture include a GCS below 9, haemodynamically unstable, active seizures or post-ictal.
90
What is the management for encephalitis?
--> Intravenous antiviral medications are used to treat the suspected or confirmed underlying cause: --> Empirical Aciclovir in suspected encephalitis treats herpes simplex virus (HSV) and varicella-zoster virus (VZV) --> Ganciclovir treats cytomegalovirus (CMV) --> Repeat lumbar puncture is usually performed to ensure successful treatment prior to stopping antivirals --> Other viral causes have no effective treatment and management is supportive. --> Followup, support and rehabilitation is required after encephalitis, with help in managing the complications.
91
What are the complications of encephalitis?
Lasting fatigue and prolonged recovery Change in personality or mood Changes to memory and cognition Learning disability Headaches Chronic pain Movement disorders Sensory disturbance Seizures Hormonal imbalance
92
What is Herpes Zoster?
Shingles ● Painful rash caused by reactivation of a nerve infection caused by the varicella-zoster virus
93
What is the pathophysiology of herpes zoster?
First presents as chickenpox in childhood ● Varicella-Zoster remains dormant in the dorsal root ganglia ● Travels through peripheral sensory nerves to the skin ● Less contagious than primary infection
94
What are the risk factors for herpes zoster?
--> immunocompromised --> HIV --> malignancy
95
What are the signs and symptoms of herpes zoster virus?
Red, painful rash - dermatomal distribution ○ Most commonly cervical, trigeminal, thoracic and lumbar dermatomes ● Fluid-filled blisters ● Stabbing or burning pain ● Fever, headache, fatigue ● Itching
96
What are the investigations for herpes zoster?
● PCR test ● CSF analysis ● Bloods & cultures ● Often a clinical diagnosis
97
What is the treatment for herpes zoster virus?
Antiviral therapy ○ Acyclovir ○ Valacyclovir ○ Famciclovir ● Immunocompromised patients should be treated with IV acyclovir ● Analgesia ● Antipyretics
98
What is Malaria?
Malaria is an infectious disease caused by members of the Plasmodium family of protozoan parasites. Protozoa are single-celled organisms.
99
What is the most dangerous and severe member of the plasmodium family?
Plasmodium falciparum
100
how does malaria spread?
Through the bites of female anopheles mosquitoes
101
What are the different types of malaria?
Plasmodium falciparum is the most severe and dangerous form Plasmodium vivax Plasmodium ovale Plasmodium malariae
102
Describe the life cycle of malaria
Malaria is spread by female Anopheles mosquitoes, most commonly at night time. Infected blood is sucked up by feeding mosquitoes. Malaria in the blood reproduces in the gut of the mosquito producing thousands of sporozoites (malaria spores). When that mosquito bites another human or animal the sporozoites are injected by the mosquito. These sporozoites travel to the liver of the newly infected person. They can lie dormant as hypnozoites for several years in P. vivax and P. ovale. They mature in the liver into merozoites which enter the blood and infect red blood cells. In red blood cells, the merozoites reproduce over 48 hours, after which the red blood cells rupture releasing loads more merozoites into the blood and causing haemolytic anaemia. This is why people infected with malaria have high fever spikes every 48 hours.
103
What is the presentation of malaria?
Symptoms occur from 6 months post-infection P. vivax and P. ovale commonly present 6 months post-infection Non-specific Symptoms -->Fever, sweats and rigors --> Malaise --> Myalgia --> Headache --> Vomiting Signs --> Pallor due to the anaemia --> Hepatosplenomegaly --> Jaundice as bilirubin is released during the rupture of red blood cells Severe disease in P. falciparum --> Shortness of breath --> Fits and hypovolaemia --> AKI and nephrotic syndrome
104
How is malaria diagnosed?
--> Travel history --> Thick and thin blood smears A negative film can be seen If negative, 2 more films should be sent over the next 48 hours --> Rapid diagnostic tests Detect parasitic antigens --> PCR --> FBC, LFTs, U&Es, blood gases, blood culture --> CXR, lumbar puncture
105
What is the management of malaria?
Treatment: - Uncomplicated falciparum: artemisinin-based combination (Artemether with lumefantrine) therapy - Uncomplicated non-falciparum: artemisinin-combination therapy or chloroquine (many strains of malaria are now resistant to chloroquine) - Severe falciparum: IV artesunate or IV quinine dihydrochloride Do not treat those with G6PD deficiency Need specialist help
106
What are the complications of Plasmodium Falciparum malaria infection?
Cerebral malaria Seizures Reduced consciousness Acute kidney injury Pulmonary oedema Disseminated intravascular coagulopathy (DIC) Severe haemolytic anaemia Multi-organ failure and death
107
Give an example of a benign and highly malignant brain tumour
Meningioma - benign Glioblastoma - highly malignant
108
What is the presentation of brain tumours?
--> focal neurological symptoms as they develop, depends where the tumour is --> often present with signs and symptoms of raised ICP - headaches - Altered mental state - Visual field defects - Seizures (particularly focal) - Unilateral ptosis - Third and sixth nerve palsies - Papilloedema (on fundoscopy)
109
a patient that has had an unusual change in personality and behaviour where might a brain tumour be present based on the presentation?
The frontal lobe as this lobe is responsible for personality and high-level decision making
110
What are some potential causes of increased ICP?
Brain tumours Intracranial haemorrhage Idiopathic intracranial hypertension Abscesses or infection
111
List some concerning features of a headache that should prompt further investigations.
Constant Nocturnal Worse on waking Worse on coughing, straining or bending forward Vomiting
112
What is papilloedema and what does it represent
--> Papilloedema is a swelling of the optic disc secondary to raised intracranial pressure --> The sheath around the optic nerve is connected with the subarachnoid space. --> CSF under high pressure can flow into the optic nerve sheath. --> increases the pressure around the optic nerve where it connects with the back of the eye at the optic disc, --> causing optic disc swelling. --> This can be seen on fundoscopy examination. - retinal vessels are able to flow straight across a flat surface, whereas they will curve over a raised disc.
113
What are the common cancers that metastasise to the brain?
- Lung - Breast - Renal cell carcinoma - Melanoma
114
What are gliomas?
Gliomas are tumours of the glial cells in the brain or spinal cord. There are three types to remember (listed from most to least malignant): Astrocytoma (glioblastoma multiforme is the most common) Oligodendroglioma Ependymoma
115
What are meningiomas?
Meningiomas are tumours growing from the cells of the meninges in the brain and spinal cord. They are usually benign, however, they take up space and this mass effect can lead to raised intracranial pressure and neurological symptoms.
116
Are pituitary tumours usually benign or malignant?
--> Benign
117
What is the problem if pituitary tumours become large enough?
They can press on the optic chiasm and cause bilateral hemianopia
118
What are the signs and symptoms of pituitary tumours and why might they occur?
--> Compression of optic chiasm - bilateral hemianopia --> They have the potential to cause hormone deficiencies or to release excessive hormones which can lead to: - Acromegaly - Hyperprolactinaemia - Cushing’s disease - Thyrotoxicosis
119
What is the management of brain tumours?
Management options include: Palliative care Chemotherapy Radiotherapy Surgery - dependent on the grade and behaviour of the brain tumour
120
What is the treatment for pituitary adenomas?
Trans-sphenoidal surgery Radiotherapy Bromocriptine to block prolactin-secreting tumours Somatostatin analogues (e.g. octreotide) to block growth hormone-secreting tumours
121
What are acoustic neuromas?
Acoustic neuromas are benign tumours of the Schwann cells surrounding the auditory nerve (vestibulocochlear nerve) that innervates the inner ear.
122
Where do acoustic neuromas normally form?
cerebellopontine angle
123
Are acoustic neuromas normally bilateral or unilateral?
Unilateral
124
What are bilateral acoustic neuromas associated with?
Neurofibromatosis type 2 - a genetic condition that causes tumours to grow along your nerves
125
What is the presentation of acoustic neuromas?
The typical patient is aged 40-60 years presenting with a gradual onset of: Unilateral sensorineural hearing loss (often the first symptom) Unilateral tinnitus Dizziness or imbalance A sensation of fullness in the ear Can be a presentation of facial nerve palsy
126
What are the investigations for acoustic neuromas?
--> Audiometry is used to assess hearing loss. There will be a sensorineural pattern of hearing loss. --> CT/MRI - establish the diagnosis and features of the tumour. MRI provides more detail than CT.
127
What is the management of acoustic neuromas?
ENT specialist management options include: --> Conservative management with monitoring may be used if there are no symptoms or treatment is inappropriate --> Surgery to remove the tumour (partial or total removal) --> Radiotherapy to reduce the growth
128
What are the risks associated with acoustic neuroma treatment?
--> Vestibulocochlear nerve injury, with permanent hearing loss or dizziness --> Facial nerve injury, with facial weakness
129
What is bulbar palsy?
Bulbar palsy refers to a set of signs and symptoms linked to the impaired function of the lower cranial nerves, typically caused by damage to their lower motor neurons or to the lower cranial nerve itself. The impacted cranial nerves are a set of nerves that arise straight from the brainstem and include cranial nerves IX (9), X (10), XI (11), and XII (12). Lower motor neurons are the neurons that connect the central nervous system, such as the brain and spinal cord, to the muscles they innervate
130
What is the difference between progressive and non-progressive bulbar palsy?
--> Progressive bulbar palsy is more common and refers to the escalation of symptoms over time. It can occur in both children and adults. --> Non-progressive bulbar palsy, on the other hand, refers to bulbar palsy that does not worsen; it is considered very uncommon
131
What is the difference between bulbar palsy and pseudobulbar palsy?
--> share many of the same symptoms, --> Pseudobulbar palsy (damage to the upper motor neurons) is often characterized by the atypical expression of emotion displayed by unusual outbursts of laughing or crying, called emotional lability. --> Bulbar palsy, an individual’s emotions usually remain unaffected. --> Pseudobulbar palsy includes the absence of facial emotions, a spastic and pointed tongue, and an exaggerated jaw jerk.
132
Which cranial nerves are affected in bulbar palsy?
9, 10, 11 and 12
133
What are the signs and symptoms of bulbar palsy?
--> Cranial nerve IX (the glossopharyngeal nerve) is involved in salivation, swallowing, and the gag reflex. --> If cranial nerve IX is injured, it can lead to difficulty swallowing (dysphagia) and a reduced gag reflex. --> Common signs and symptoms of damage to the other cranial nerves include difficulty chewing, nasal regurgitation, slurred speech, difficulty in handling secretions, aspiration of secretions, altered vocal ability (dysphonia) and difficulty articulating words (dysarthria), reduced gag reflex, drooling, difficulty chewing, difficulty with consonants, atrophic tongue, weak jaw/facial muscles, normal or absent jaw jerk reflex
134
What are the possible causes of bulbar palsy?
Most common: - Brainstem stroke (especially lateral medullary syndrome) - Brainstem tumour Other causes: - Motor neuron disease - GBS
135
What are the investigations for bulbar palsy?
--> Clinical diagnosis based on history --> CSF analysis to rule out MS --> MRI to diagnose a brainstem stroke or tumour
136
What is the treatment for bulbar palsy?
--> No known treatment --> Supportive treatment - medications to stop drooling, feeding tube to help with dysphagia, speech and language therapy to help with speech, chewing and swallowing --> Other specific treatments based on the cause
137
What is the cerebellum responsible for?
The cerebellum is the region of the brain responsible for controlling stance, gait, and balance, as well as the coordination of complex and goal-directed movements
138
What are the causes of cerebellar syndrome?
Acute --> Infarction, TIA --> Head trauma, oedema, haemorrhage --> Infections (acute postviral cerebellitis), including: Adults: VZV, EBV, Lyme disease, tertiary syphilis, malaria, prion diseases (e.g., Creutzfeldt-Jakob disease) Children: VZV, coxsackievirus, parvovirus B19, HHV-6, hepatitis A, enteroviruses, measles, mumps, Lyme disease, etc. --> Medication, toxins, and poisons: barbiturates, benzodiazepines, heavy metals, and chemotherapy Subacute and chronic --> Alcoholism --> Intracranial tumours (e.g., medulloblastoma) --> Vitamin deficiencies: vitamin B12 deficiency, vitamin B1 deficiency (Wernicke encephalopathy) --> Paraneoplastic cerebellar degeneration --> Genetic: Friedreich ataxia, ataxia telangiectasia, spinocerebellar ataxia, --> Multiple sclerosis --> Wilson disease (rare)
139
What is the presentation of cerebellar syndrome?
DANISH - Dysdiadochokinesis - Inability to perform rapidly alternating agonistic-antagonistic movements - Ataxia - coordination balance and speech - gait - Nystagmus - Intention tremor - finger-to-nose test with shaky hands - Scanning speech, dysarthria - words are broken down into separate syllables and spoken with varying force - Hypotonia, hyporeflexia cerebellar drift - pronator drift
140
What are the investigations for cerebellar syndrome?
Neuroimaging (CT/MRI): indicated to rule out infarction, haemorrhage, tumours, oedema Laboratory testing: complete blood cell count; electrolytes, vitamin B12 levels, vitamin B1 levels Genetic testing: if other diagnostic tests are negative or inconclusive
141
What is the management of the cerebellar disorder?
treat the underlying cause
142
What is Bell's palsy?
Lower motor neuron weakness of cranial nerve VII (facial nerve) → acute peripheral facial palsy
143
What is the facial nerve pathway and what are the five branches?
--> exits the brainstem at cerebellopontine angle --> passes through the temporal bone and parotid gland --> then divides into five branches Temporal Zygomatic Buccal Marginal mandibular Cervical
144
What are the three functions of the facial nerve?
motor - It supplies the muscles of facial expression, the stapedius in the inner ear and the posterior digastric, stylohyoid and platysma muscles in the neck Sensory - It carries taste from the anterior 2/3 of the tongue. parasympathetic - It provides the parasympathetic supply to the: Submandibular and sublingual salivary glands Lacrimal gland (stimulating tear production)
145
how can you distinguish between upper and lower motor neurone bell's palsy?
--> Each side of the forehead has upper motor neurone innervation by both sides of the brain. However, each side of the forehead only has lower motor neurone innervation from one side of the brain --> In an upper motor neurone lesion, the forehead will be spared, and the patient can move their forehead on the affected side. - should be referring for suspected stroke. --> In a lower motor neurone lesion, the forehead will NOT be spared, and the patient cannot move their forehead on the affected side.
146
Which conditions can cause unilateral upper motor neurone facial palsy signs?
Cerebrovascular accidents (strokes) Tumours
147
Which conditions can cause biilateral upper motor neurone facial palsy signs?
Pseudobulbar palsies Motor neurone disease
148
What are the causes of Bell's palsy?
idiopathic Thought to be related to inflammation and oedema of the facial nerve secondary to viral infection or autoimmunity
149
What is the presentation of Bell's palsy?
symptoms Presents with rapid onset (<72 Hours) of unilateral facial weakness post-auricular/ear pain Difficulty chewing incomplete eye closure drooling tingling in cheek/mouth hyperacusis - decrease in everyday sound tolerance Non-forehead sparing symptoms ocular dryness decreased taste Asymmetrical smile Drooping of the corner of the mouth Drooping of the eyebrow
150
What are the investigations for Bell's palsy?
Clinical diagnosis - based on unilateral facial weakness, of rapid onset, without forehead sparing (with forehead sparing suspected UMN lesion) → may include routine blood tests, neuroimaging, specialist tests e.g lumbar puncture → consider HIV test
151
What is the management of Bell's palsy?
Treatment → Management largely supportive, but prednisolone may be used in those presenting within 72 hours of onset. antiviral treatment e.g acyclovir can be considered → eye care - lubricating drops, taping eye when sleeping, sunglasses outdoors, referral to ophthalmology considered
152
What is epilepsy?
Epilepsy is an umbrella term for a condition where there is a recurrent tendency to have seizures - chronic
153
What are seizures?
Seizures are transient episodes of abnormal electrical activity in the brain. There are many different types of seizures. spontaneous and intermittent
154
What is ictus?
The epileptic attack itself
155
What is prodrome in epilepsy?
Nonspecific symptoms that precede an epileptic attack
156
What is aura in epilepsy?
Sensory disturbances that precede an attack, usually by minutes. More specific.
157
What are the potential causes/risk factors of epilepsy?
Family history – Idiopathic Premature birth Developmental abnormalities Trauma Drugs – cocaine Space occupying lesion – tumour, infection, haematoma
158
What are the two main types of seizures?
--> Primary generalised - 30/40% --> partial/focal - 60-70%
159
What are primary generalised seizures and what presentation are they associated with?
- Originates in the midbrain or brainstem - Electrical discharge in both hemispheres - Associated with LOC or awareness
160
What are focal/partial seizures?
--> Focal onset, an electrical discharge is restricted to one area of the brain --> It may develop into a generalised (secondary)
161
Name the different types of generalised seizures
--> Generalised tonic-clonic seizures --> tonic seizures --> clonic seizures --> Absence seizures --> atonic seizures --> myoclonic seizures
162
What are generalised tonic-clonic seizures (grand-mal)?
--> Often no aura --> tonic phase - rigid, tongue biting, incontinence, no breathing during the phase --> Clonic phase - convulsions, limb jerking, eye-rolling, uncoordinated breathing --> self - limiting --> Physical injuries are common --> prolonged post-ictal phase - confused, drowsy, irritable
163
What are tonic seizures?
--> high tone --> Rigid stiff limbs --> no limb jerking
164
What are clonic seizures?
--> seizures with muscle jerking
165
what are absence seizures?
--> patient becomes blank, stares into space and then abruptly returns to normal
166
What are atonic (akinetic) seizures?
--> sudden loss of muscle tone and movement and they fall --> also known as drop attacks
167
What are myoclonic seizures?
--> Sudden brief muscle contractions
168
What are the different types of partial/focal seizures?
--> Simple partial seizure --> Complex partial seizure --> partial seizures with secondary generalisation
169
What is a simple partial seizure?
--> No loss of consciousness --> No post-ictal signs --> isolated limb jerking --> Head turning away from the side of the seizure --> isolated paraesthesia --> Todd's paralysis - temporary paralysis/weakness
170
What is a complex partial seizure?
--> most commonly in the temporal lobe --> can affect awareness/memory before during or after --> Visual/auditory hallucinations --> lip-smacking - automatism --> Post-ictal confusion/drowsiness is common
171
what are partial seizures with secondary generalisation?
--> partial seizures that spread to the lower brain areas which initiate a generalised seizure --> usually tonic-clonic --> 2/3rds with partial seizures develop generalised seizures
172
if there is a focal seizure in the temporal lobe what presentation might be seen?
Speech comprehension, memory and emotion are affected Anxiety Automatisms = lip-smacking
173
if there is a focal seizure in the frontal lobe what presentation might be seen?
Motor disturbances Jacksonian march = up and down the motor homunculus Postictal Todd’s palsy
174
if there is a focal seizure in the parietal lobe what presentation might be seen?
sensation Occipital = vision ( visual phenomena = spots, lines, flashes)
175
What are the investigations for epileptic seizures?
EEG = supports the diagnosis MRI/ CT head = exclusion of space-occupying lesions Blood to rule out metabolic disturbances
176
What is the epilepsy management
- Generalised Tonic-Clonic = 1st line: Sodium Valproate (males) & Lamotrigine or Levetiracetam (females) - Tonic/atonic = Sodium Valproate (males) & Lamotrigine (females) - Myoclonic = Sodium Valproate (males) & Levetiracetam (women) - Absence = 1st line: Ethosuximide 2nd line: Sodium Valproate (male) & Lamotrigine or levetiracetam (female) NB - Carbamazepine may exacerbate absence seizure - Partial (focal) = 1st line: Lamotrigine or Levetiracetam 2nd line: Carbamazepine
177
What is status epilepticus and what is the treatment?
a continuous seizure lasting over 5 minutes or repeated seizures with no recovery in between. IV Lorazepam ( first line), if ineffective Phenytoin
178
What are the signs of a non-epileptic seizure?
Metabolic disturbances ( low sodium, hypoxia) Longer Don't occur in sleep No incontinence + tongue biting Pre ictal anxiety signs No muscle pain
179
What are febrile convulsions?
type of seizure that occurs in children with a high fever
180
in which age group do febrile convulsions occur?
between 6 months and 5 years
181
What type of seizures are seen in simple febrile convulsions?
generalised tonic-clonic seizures last less than 15 minuets only occur once in a single febrile illness
182
When can febrile convulions be described as complex febrile convulsions?
when they consist of partial or focal seizures, lasting more than 15 minutes or occur multiple times during the same febrile illness
183
What are the management/investigations for febrile convulsions?
Rule out differentials complex febrile convulsions may need extra investigations treat the underlying cause e.g infection
184
What are the differentials of febrile convulsions?
Epilepsy Meningitis, encephalitis or another neurological infection such as cerebral malaria Intracranial space occupying lesions, for example, brain tumours or intracranial haemorrhage Syncopal episode Electrolyte abnormalities Trauma (always think about non-accidental injury)
185
What is cerebral palsy?
--> Permanent neurological problems resulting from damage to the brain around the time of birth --> not a progressive condition
186
What are the causes of cerebral palsy?
Antenatal --> maternal infections --> Trauma during pregnancy perinatal --> Birth asphyxia --> pre-term birth postnatal --> meningitis --> Severe neonatal jaundice --> head injury
187
What are the different types of cerebral palsy?
Spastic --> hypertonia and reduced function due to damage to the upper motor neurones dyskinetic --> problems controlling muscle tone, with hypertonia and hypotonia, from damage to the basal ganglia ataxic --> problems with coordinated movement resulting from damage to the cerebellum mixed --> a mix
188
What are mono/hemi/di and quadriplegic spastic cerebral palsy?
Monoplegia: one limb affected Hemiplegia: one side of the body affected Diplegia: four limbs are affected, but mostly the legs Quadriplegia: four limbs are affected more severely, often with seizures, speech disturbance and other impairments
189
What is the presentation of cerebral palsy?
--> become evident during development --> Failure to meet milestones --> Increased or decreased tone, generally or in specific limbs --> Hand preference below 18 months is a key sign to remember for exams --> Problems with coordination, speech or walking --> Feeding or swallowing problems --> Learning difficulties --> Upper motor/lower motor, inspection, tone, power and reflex signs --~> gait abnormalities
190
What is the management of cerebral palsy?
--> no cure, management of symptoms --> Management involves a multi-disciplinary team approach --> physio --> occupational therapy --> Speech and language therapy --> dieticians --> orthopaedic surgeons --> Muscle relaxants for spasticity, epileptic drugs and drugs for excessive drooling can be given --> social workers
191
What is hypoxic-ischaemic encephalopathy?
occurs in neonates as a result of hypoxia during birth hypoxia- lack of oxygen ischaemia - restriction of blood to the brain encephalopathy - malfunctioning of the brain --> can lead to permanent damage and cerebral palsy
192
What are the causes of hypoxic-ischaemic encephalopathy?
anything that leads to asphyxia - Maternal shock - Intrapartum haemorrhage - Prolapsed cord, causing compression of the cord during birth - Nuchal cord, where the cord is wrapped around the neck of the baby
193
How can hypoxic-ischaemic encephalopathy be staged and what is the staging called?
--> Sarnat staging Mild: -->Poor feeding, general irritability and hyper-alert --> Resolves within 24 hours --> Normal prognosis Moderate: --> Poor feeding, lethargy, hypotonic and seizures --> Can take weeks to resolve --> Up to 40% develop cerebral palsy Severe: --> Reduced consciousness, apnoeas, flaccid and reduced or absent reflexes --> Up to 50% mortality --> Up to 90% develop cerebral palsy
194
What is the management of Hypoxic-ischaemic encephalopathy?
--> Supportive care - neonatal resuscitation/ ventilation/ seizure treatment --> Therapeutic hypothermia - to help protect the brain from hypoxic injury - reduces inflammation --> MDT involvement for any lasting disability
195
What is an extradural haemorrhage?
Collection of blood between the dura mater and the bone is usually caused by head injury
196
When should an extradural haemorrhage be suspected?
After a traumatic head injury with low consciousness levels or slow to improve or lucid interval
197
What are the common causes of an extradural haemorrhage?
--> most commonly due to head trauma resulting in a fracture of the temporal or parietal bone causing a rupture in the middle meningeal artery
198
In whom do extradural haemorrhages occur most often?
Young adults
199
What is the typical presentation of an extradural haemorrhage?
--> head injury --> Brief LOC or drowsiness --> Lucid interval - period of improved neurological symptoms and consciousness followed by a rapid decline over hours as the haematoma gets large enough to compress the intracranial contents --> followed by a rapid decline, sever headache, vomiting, confusion, seizures, raised ICP - cushings reflex - triad of hypertension, bradycardia, irregular breathing, physiological response to raised ICP to attempt to improve perfusion
200
What are the differentials for an extradural haemorrhage?
--> Subarachnoid haemorrhage --> subdural haemorrhage --> meningitis
201
What is the gold standard investigation for an extradural haemorrhage?
CT head --> shows a hyperdense biconcave region, limited by the cranial sutures, lemon shape
202
What is the management for an extradural haemorrhage?
--> ABCDE assessment --> IV mannitol - reduce ICP --> Neurosurgery - Clot evacuation - burr hole craniotomy, ligation of the middle meningeal artery --> may need incubation or ventilation
203
What is a subarachnoid haemorrhage?
Spontaneous bleeding between the arachnoid and pia mater, usually due to a rupture of a cerebral aneurysm, mainly in the communicating arteries in the circle of willis
204
What is the prognosis of a subarachnoid haemorrhage?
High mortality (50% die straight away), 10-20% more from rebleeding, 50% left with significant disability
205
What are the risk factors for subarachnoid haemorrhage?
--> Hypertension --> Known aneurysm --> Previous SAH --> Smoking --> Alcohol --> FHx --> cocaine --> sickle cell anaemia Bleeding disorders --> PKD --> Coarctation of the aorta --> Connective tissue disorders - ED --> associated with berry aneurysms
206
What are the causes of a subarachnoid haemorrhage?
- Traumatic injury - Aneurysmal rupture - berry (70-80%) at communicating branches - AV malformations - an abnormal artery and venous connections (15% of cases) - Idiopathic
207
What is the pathophysiology of subarachnoid haemorrhages?
Tissue ischaemia - due to bleeding loss, causing cell death Raised ICP - Blood into cranial space, space-occupying lesion Blood-causing meningism - could obstruct CSF outflow (hydrocephalus) Vasospasm - bleeding irritates other vessels causing ischaemic injury
208
What are the symptoms of someone with subarachnoid haemorrhage?
Thunderclap headache - typically occipital, excruciating Sentinel headache - Before the main rupture, early sign - 6% cases - Nausea, vomiting, seizures, visual disturbance, LoC, photophobia
209
What are the signs of someone with a subarachnoid haemorrhage?
- Meningeal irritation - Neck stiffness, Kernig's (leg raise - pain), Brudzinski (neck raise - hip\knee flexion) - Retinal, vitreous and subhyaloid bleeds w/ or without papilloedema - Focal neurological signs - e.g. 3rd nerve palsy - Increased BP
210
What are the investigations for a subarachnoid haemorrhage?
Immediate CT head - detects >95%, star-shaped sign Lumbar puncture - if normal ICP, after 12 hours (xanthochromia - confirms SAH, raised red cells) MR/CT angiography - establish source, in all patients fit for surgery
211
Whi is a lumbar puncture contraindicated with raised ICP?
coning risk
212
What is the treatment for subarachnoid haemorrhages?
--> ABCDE assessment --> IV fluids - maintains cerebral perfusion --> Nimodipine - Ca2+ antagonist, reduces the risk of vasospasm --> neurosurgery - endovascular coiling or surgical clipping, ventricular draining - hydrocephalus
213
What is the physiological response to increased ICP called?
Cushing's reflex - triad of hypertension, bradycardia, irregular breathing, physiological response to raised ICP to attempt to improve perfusion
214
What is a subdural haematoma?
Accumulation of blood between the arachnoid and dura mater, usually due to the rupture of a vein (bridging veins) . Can be acute or chronic.
215
What are the risk factors for subdural haematoma?
--> more common in elderly and alcoholics (brain atrophy and falls risk) --> Co-morbidities that make the patient more vulnerable to falls - dementia and delirium --> most due to trauma --> anticoagulation --> history of coagulopathy --> history of LOC
216
What are the risk factors for subdural haematomas?
--> More common in the elderly and alcoholics (brain atrophy and increased falls) --> Most due to trauma --> Anticoagulation --> Co-morbidities that make a patient more vulnerable to falls - dementia and delirium --> history of coagulopathy --> history of LOC
217
What are the risk factors for subdural haematomas?
--> More common in the elderly and alcoholics (brain atrophy and increased falls) --> Most due to trauma --> Anticoagulation --> Co-morbidities that make a patient more vulnerable to falls - dementia and delirium --> history of coagulopathy --> history of LOC
218
What is the pathophysiology of subdural haematomas?
--> Bleeding from bridging veins into subdural space --> forms a haematoma which stops the bleeding --> weeks/months later the clot autolyses - clot draws water in and expands --> Radual increase in ICP - midline shift - herniation and coming - coma and death
219
What is the presentation of a patient with a subdural haematoma?
Fluctuating consciousness Drowsiness Headache Confusion Behavioural change Signs of ICP – vomiting, nausea, seizure, raised BP, Cushing's triad (bradycardia, hypertension and irregular breathing) Coma – many present with this GRADUAL DETERIORATION
220
What are the investigations for a subdural hematoma?
--> CT head - acute: hyperdense crescent-shaped area/ chronic: hypodense crescent shape, not limited to cranial sutures
221
What is the management of a subdural hematoma?
Starts with basics – ABCDE, Start oxygen, Maintain systolic BP >90 mmHg Neurosurgery: Burr hole – irrigation + evacuation Craniotomy – to reduce ICP acutely Address cause for fall – arrhythmias, cataracts IV mannitol – reduce ICP
222
What are the two major categories of stroke?
Ischaemic stroke (87%) Haemorrhagic stroke (13%)
223
in Ischaemic strokes what can cause disruption of blood supply?
Thrombus formation or embolus, for example in patients with atrial fibrillation Atherosclerosis Shock Vasculitis systemic hypoperfusion - cardiac arrest
224
What is an ischaemic stroke?
Caused by occlusion of blood vessels by a clot. Infarcted area dies causing permanent deficit, penumbra surrounding may regain function with recovery.
225
What are the causes of an ischaemic stroke?
Aetiology: Anything that increases the risk of an embolus forming Atherothromboembolism - e.g. from the carotid artery Cardioembolism - AF, post MI, valve disease, IE Hyperviscosity syndrome - e.g. Waldenstrom’s macroglobulinemia, polycythaemia vera Hypoperfusion - systemic blood loss Vasculitis Fat emboli - long bone fracture Venous sinus thrombosis - infection, injury, pregnancy, inflammatory conditions (very rare only 1%)
226
What are the risk factors of an ischaemic stroke?
--> Increasing age >65 --> Hypertension --> Smoking Male Diabetes Recent/past TIA Hyperlipidaemia Heart disease - IHD, AF, valve disease Peripheral vascular disease Clotting disorder Vasculitis Alcohol Infective endocarditis Carotid bruit - stenosis Black, Asian
227
What are the investigations of an ischaemic stroke?
Immediate CT scan - Distinguish ischaemic from haemorrhagic, shows site of infarct, may be negative in first few hours Diffusion-weighted MRI - gold More sensitive, for a confirmed diagnosis Blood tests - Glucose (rule out hypoglycaemia), FBC (polycythaemia), ESR (vasculitis), U&Es, cholesterol, INR (if on warfarin) ECG - In AF or MI Carotid ultrasound - carotid stenosis - endarterectomy to remove plaques
228
What is the classification system for strokes?
Bamford stroke classification
229
What is the Bamford stroke classification?
230
What is the Bamford stroke classification?
This system categorises stroke based on the initial presenting symptoms and clinical signs. This system does not require imaging to classify the stroke, instead, it is based on clinical findings alone.
231
Bamford stroke classification - what is total anterior circulation stroke and what is the criteria for this
A total anterior circulation stroke (TACS) is a large cortical stroke affecting the areas of the brain supplied by both the middle and anterior cerebral arteries. All three of the following need to be present for a diagnosis of a TACS: Unilateral weakness (and/or sensory deficit) of the face, arm and leg Homonymous hemianopia Higher cerebral dysfunction (dysphasia, visuospatial disorder)
232
Bamford stroke classification - what is a posterior-anterior circulation stroke and what is the criteria for this
A partial anterior circulation stroke (PACS) is a less severe form of TACS, in which only part of the anterior circulation has been compromised. Two of the following need to be present for a diagnosis of a PACS: Unilateral weakness (and/or sensory deficit) of the face, arm and leg Homonymous hemianopia Higher cerebral dysfunction (dysphasia, visuospatial disorder)* *Higher cerebral dysfunction alone is also classified as PACS.
233
Bamford stroke classification - what is posterior circulation syndrome and what are the criteria for this
A posterior circulation syndrome (POCS) involves damage to the area of the brain supplied by the posterior circulation (e.g. cerebellum and brainstem). One of the following need to be present for a diagnosis of a POCS: Cranial nerve palsy and a contralateral motor/sensory deficit Bilateral motor/sensory deficit Conjugate eye movement disorder (e.g. horizontal gaze palsy) Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia) Isolated homonymous hemianopia
234
Bamford stroke classification - what is a lacunar stroke and what are the criteria for this
A lacunar stroke (LACS) is a subcortical stroke that occurs secondary to small vessel disease. There is no loss of higher cerebral functions (e.g. dysphasia) One of the following needs to be present for a diagnosis of a LACS: Pure sensory stroke Pure motor stroke Sensorimotor stroke Ataxic hemiparesis
235
What area of the brain does the anterior cerebral artery supply?
anteromedial area of the cerebrum
236
What area of the cerebrum does the middle cerebral artery supply?
majority of the lateral cerebrum
237
What area of the cerebrum do the posterior cerebral arteries supply?
a mixture of the medial and lateral areas of the posterior cerebrum
238
What is the Glasgow coma scale (GCS)?
allows healthcare professionals to consistently evaluate the level of consciousness of a patient. It is commonly used in the context of head trauma, but it is also useful in a wide variety of other non-trauma related settings. Regular assessment of a patient’s GCS can identify early signs of deterioration.
239
What are the three aspects of behaviour that are independently measured as part of an assessment of a patient's GCS?
motor responsiveness, verbal performance and eye-opening. The highest response from each category elicited by the healthcare professional is scored on the chart.
240
What is the highest and lowest score on GCS?
15 highest 3 lowest - coma or dead
241
What is the scoring system for eye-opening in GCS?
Eye-opening spontaneously 4 points Eye-opening to sound 3 points Eye-opening to pain 2 points No response 1 point Not testable NT
242
What is the scoring system for verbal response in GCS?
Orientated 5 points Confused conversation 4 points Inappropriate words 3 points Incomprehensible sounds 2 points No response 1 point Not testable NT common questions - “Can you tell me your name?” “Do you know where you are at the moment?” “Do you know what the date is today?”
243
What is the scoring system for motor response in GCS?
Obeys command 6 points Localises to pain 5 points Withdraws to pain 4 points Flexion decorticate posture (abnormal flexion response to pain) 3 points Abnormal extension decerebrate posture 2 points No response 1 point Not testable NT
244
What is a transient ischaemic attack?
Acute loss of cerebral/ ocular function with sudden symptoms lasting less than 24 hours mainly due to an atherothromboembolism from an artery Temporary focal cerebral ischaemia due to lack of oxygen, no infarction
245
What are the risk factors for a TIA?
Same as IHD --> Age --> smoking --> HTN --> cardiovascular disease --> AF --> Diabetes
246
What are the causes of a transient ischaemic attack?
--> main cause atherothromboembolism - mainly from the carotid arteries --> Cardioembolism - valvular disease/prosthetic valve, after an MI or AF
247
What is the presentation of a transient ischaemic attack?
Carotid territory symptoms - 90% --> Amaurosis fugax --> aphasia --> hemiparesis --> hemisensory loss --> Hemianopic visual changes Vertebrobasilar territory symptoms - 10% --> diplopia, vertigo, vomiting --> chocking and dysarthria --> ataxia --> Hemisensory loss --> Hemianopic or bilateral visual loss --> tetraparesis --> Loss of consciousness (rare)
248
What are the investigations for a transient ischaemic attack?
→ Diffusion-weighted CT/MRI → first line → Carotid imaging with doppler ultrasound → Then MR/CT angiography if the stenosis is found → Bloods → Glucose → FBC - polycythaemia → ESR - raised in vasculitis → INR - if pt is on warfarin → U&E → Cholesterol → ECG - AF? → Echocardiogram
249
What is the management of a transient ischaemic attack?
→ immediate management → loading dose of Aspirin 300mg + refer to specialist to be seen within 24hrs of onset of sx → Antiplatelet therapy → Standard treatment is aspirin 75mg daily with MR Dipyridamole or clopidogrel daily → patients with AF → anticoagulation e.g DOAC/warfarin → carotid endarterectomy - if >70% carotid stenosis, reduces stroke and TIA risk by 75% → Control CV risk factors → BP control, Smoking cessation, Statins, no driving for 1 month
250
What is giant cell arteritis - temporal arteritis?
Giant cell arteritis is a systemic vasculitis of the medium and large arteries. It typically presents with symptoms affecting the temporal arteries and is also known as temporal arteritis. --> medical emergency as a complication is vision loss which is irreversible, high dose steroids are given immediately if a diagnosis is suspected
251
What are the risk factors for temporal arteritis GCA?
--> women --> over 50 --> Strong link with polymyalgia rheumatica 50% of patients with temporal arteritis have PMR
252
What is the pathophysiology of giant cell arteritis/ temporal arteritis?
Chronic vasculitis, characterised by granulomatous inflammation of the walls of medium and large vessels
253
What are the symptoms of GCA/temporal arteritis?
The main presenting feature is a headache: Severe unilateral headache typically around temple and forehead Scalp tenderness may be noticed when brushing hair Jaw claudication Blurred or double vision Irreversible painless complete sight loss can occur rapidly There may be associated systemic symptoms such as: Fever Muscle aches Fatigue Weight loss Loss of appetite Peripheral oedema
254
How is a diagnosis of GCA made?
--> clinical presentation --> Raised ESR --> Temporal artery biopsy - multinucleated giant cells found --> Temporal artery ultrasound may show thickening of the wall - halo sign --> FBC may show normocytic anaemia and thrombocytosis --> LFT's - raised Alkaline phosphatase --> CRP usually raised
255
What is the management of GCA?
--> medical emergency --> Urgent referral to rheumatologist/ophthalmologist if vision loss --> WITH visual symptoms - 60-100mg of prednisolone one off in primary care --> WITH visual loss - secondary care - methylprednisolone 500mg-1g of IV methylprednisolone for 3 days --> Without visual loss- 40-60mg of prednisolone per day --> aspirin - reduces risk of strokes and visual loss --> PPI for steroids
256
What are the additional measures for patients on steroids?
DON’T – Don’t stop taking steroids abruptly. There is a risk of adrenal crisis. S – Sick Day Rules. T – Treatment Card. O – Osteoporosis prevention with bisphosphonates and supplemental calcium and vitamin D. P – Proton pump inhibitor for gastric protection.
257
What are the complications of GCA?
Early neuro-ophthalmic complications: --> Vision loss --> Cerebrovascular accident (stroke) Late: --> Relapses of the condition are common --> Steroid-related side effects and complications --> Cerebrovascular accident (stroke) --> Aortitis leading to aortic aneurysm and aortic dissection
258
What are migraines?
--> recurrent throbbing headache often preceded by an aura & associated with nausea, vomiting and visual changes --> most common cause of episodic headache - recurrent --> more common in females and common onset before 40 years.
259
What are the risk factors for migraines?
--> genetics > FHx --> female --> age - majority of first migraines are in adolescence
260
What are some causes/triggers of migraines?
Mnemonic – CHOCOLATE Chocolate Hangovers Orgasms Cheese Oral contraceptives Lie-ins Alcohol Tumult ie. Loud noises Exercise no known cause - but we know the triggers
261
What is the clinical presentation of migraines?
Prodrome - yawning, cravings, mood/sleep changes Aura - precedes attack and can be a variety of symptoms, visual disturbances e.g lines, dots, zig-zags and somatosensory signs e.g paresthesia, pins and needles can be with or without aura At least 2 of: Unilateral pain (usually 4-72hrs) Throbbing-type pain Moderate>severe intensity Motion sensitivity Plus, at least 1 of: Nausea/vomiting Photophobia/phonophobia There also must be a normal examination and no attributable cause
262
What are the diagnostic criteria for migraines?
At least 2 of: Unilateral pain (usually 4-72hrs) Throbbing-type pain Moderate>severe intensity Motion sensitivity Plus, at least 1 of: Nausea/vomiting Photophobia/phonophobia There also must be a normal examination and no attributable cause
263
How can migraines be diagnosed?
--> Usually, diagnosis is made clinically with few/no investigations required; however, in certain cases, other causes for headaches must be ruled out: --> lab tests - CRP, ESR --> CT/MRI red flags ie. Indications Worst/severe headache ie. Thunderclap Change in pattern of migraine Abnormal neurological exam Onset >50yrs Epilepsy Posteriorly located headache --> Lumbar puncture indications Thunderclap headache Severe, rapid onset headache/ progressive headache/ unresponsive headache
264
What is the management of migraines?
--> Triptans eg. Sumatriptan C/I in IHD, uncontrolled HTN S/Es = arrhythmias, angina > MI --> NSAIDs eg. naproxen --> Anti-emetic eg. prochlorperazine --> AVOID opioids & ergotamine Prevention Required if >2 attacks per month OR require acute meds >2x per week Beta-blockers eg. propranolol TCAs eg. amitriptyline Anti-convulsant eg. Topiramate
265
What are the differential diagnoses for headaches?
Tension headaches Migraines Cluster headaches Secondary headaches Sinusitis Giant cell arteritis Glaucoma Intracranial haemorrhage Subarachnoid haemorrhage Analgesic headache Hormonal headache Cervical spondylosis Trigeminal neuralgia Raised intracranial pressure (brain tumours) Meningitis Encephalitis
266
What are the 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 or glaucoma) Sudden onset occipital headache (subarachnoid haemorrhage) Worse on coughing or straining (raised intracranial pressure) Postural, worse on standing, lying or bending over (raised intracranial pressure) Severe enough to wake the patient from sleep Vomiting (raised intracranial pressure or carbon monoxide poisoning) History of trauma (intracranial haemorrhage) Pregnancy (pre-eclampsia)
267
Give examples of primary headaches
- tension headaches - migraines - cluster headaches
268
What are tension headaches?
--> common type of primary headaches --> mild ache across the forehead - band like pain --> could be due to muscle aches in the frontalis, temporalis, occipitalis --> No visual changes --> Can be episodic <15 days/month or chronic >15 days/month (for at least 3 months)
269
What are the causes or associations with tension headaches?
Stress Sleep deprivation Bad posture Hunger Eyestrain Anxiety Noise - no known cause
270
What is the clinical presentation of tension headaches?
Usually at least one of the following: Bilateral Pressing/tight & non-pulsatile (like an elastic band) Mild/moderate intensity +/- scalp tenderness No aura, vomiting or sensitivity to head movement Can be some “pressure” behind eyes, but pain isn’t localised to be around the eye
271
What is the management for tension headaches?
Avoidance of triggers & stress relief Symptomatic relief Aspirin Paracetamol Ibuprofen AVOID OPIOIDS Limit analgesics to no more than 6 days per month to reduce the risk of medication-overuse headaches
272
What are cluster headaches?
Episodic headaches lasting from 7 days up to 1 year, usually a couple of weeks with pain free periods between that last around 4 weeks --> considered the most disabling primary headache --> rarer than migraines and more common in males --> typically affects adults with onset usually 20-40 years
273
What are the risk factors for cluster headaches?
Smoker Alcohol male genetics - autosomal dominant gene has a link.
274
What is the clinical presentation of cluster headaches?
Rapid onset of excruciating pain, classically around the eye however other common areas are the temples or forehead Pain is strictly unilateral and localised to one area It rises to a crescendo over a few minutes and last for 15-160 minutes, once or twice a day usually around the same time of day Ipsilateral autonomic features: Watery & bloodshot eye Facial flushing Rhinorrhoea (blocked nose) Miosis (pupillary constriction) +/- ptosis (seen in 20%)
275
What is the management of cluster headaches?
Acute attacks Analgesics are unhelpful 15L 100% O2 for 15 mins via non-rebreather mask Triptans eg. Sumatriptan Prevention Verapamil (CCB) = 1st line prophylaxis Prednisolone Reduce alcohol consumption & stop smoking
276
What are secondary headaches?
Those caused by organic pathology
277
Give examples of secondary headaches
Giant cell/temporal arteritis Sentinel headache Thunderclap headache Headache of a morning Trauma Medication overuse Trigeminal neuralgia Systemic infection Meningitis/encephalitis
278
What is trigeminal neuralgia?
Episodes of acute severe facial nerve pain within the distribution of the trigeminal nerve, rare condition most common in women
279
What are some of the causes of trigeminal neuralgia?
→ vascular compression, the most common cause of trigeminal neuralgia → compressions caused by other lesions e.g meningioma → Multiple sclerosis can lead to Trigeminal neuralgia due to demyelination of the trigeminal nerve → can be idiopathic
280
What are the risk factors for trigeminal neuralgia?
→ female sex → advancing age → multiple sclerosis → FHx
281
What are the signs and symptoms of trigeminal neuralgia?
→ Short-lived episodes (seconds to minutes) of electric shock pain in the distribution of the trigeminal nerve → attacks may be recurrent and triggered by things such as cold air or eating
282
How is the diagnosis of trigeminal neuralgia made?
CT/MRI - identify lesion/vascular compression clinical diagnosis - pain lasts form a fraction of a second to 2 minutes and is severe and electric shock-like/stabbing or sharp in quality which precipitates by innocuous stimuli within the affected trigeminal distribution → rule out other conditions - jaw or dental problems, cluster headaches, post-herpetic neuralgia – a type of nerve pain linked to shingles
283
What is the treatment of trigeminal neuralgia?
→ Carbamazepine - mainstay of management → second line → gabapentin/lamotrigine → Surgical → Microvascular decompression
284
What are the three branches of the trigeminal nerve?
--> Ophthalmic - provides sensation to the forehead, anterior scalp, nose and eyes - the conjunctiva --> Maxillary - Provides sensation to the mid-face, lower eyelid, nasal cavity, palate, upper lip and maxillary teeth --> mandibular - Provides sensation to part of the scalp, part of the ear, lower face, tongue, the floor of the mouth and mandibular teeth. Provides motor input to the muscles of mastication (temporalis, masseter, medial and lateral pterygoids) and the tensor tympany
285
What are some red flags for trigeminal neuralgia?
Bilateral pain is considered a red flag Onset before 40 years Hearing difficulties or other ear problems Sensory changes Previous skin/oral lesions that could exhibit perineurally Isolated involvement of ophthalmic division Bilateral symptoms Optic neuritis Family history of multiple sclerosis
286
Why does Horner's syndrome occur?
Lesion on the sympathetic chain supplying the eye
287
What does the sympathetic nervous system innervate in the eye
Dilator pupillae: involved in mydriasis or dilation of the pupil Superior tarsal (or Muller’s) muscle: aids in elevating the upper eyelid with the levator palpebrae superioris Sweat glands THINK HORNERS
288
What's Horner's triad?
Horner’s syndrome is characterised by the triad of ptosis (drooping eyelid), anhidrosis (lack of sweating) and miosis (constricted pupil) on the ipsilateral side
289
What are some potential causes of Horner's syndrome?
Isolated injury systemic disease process
290
What are the investigations for Horner's syndrome?
The presence of systemic features with Horner’s can help guide the identification of lesion location and inform further investigations. For example, patients with cough and weight loss should undergo a chest X-ray to screen for a Pancoast tumour. For unclear cases, Horner’s can be diagnosed pharmacologically using eye drops. - apraclonidine - reverses pupillary constriction due to antagonistic effects on alpha 2 receptors
291
What is the management for Horner's syndrome?
Like investigations, the management of Horner’s depends on the underlying cause. Accurate and timely investigation of sudden-onset Horner aids in reducing morbidity and mortality of patients.
292
What are the causes of spinal cord compression?
Central disc protrusion (mostly lumbar) – often due to disc degeneration Tumour/haematoma/abscess Trauma
293
What is the presentation of spinal cord compression?
Myelopathic - affects the entire spinal cord Motor deficit below the level of compression – generally UMN pattern if gradually progressive Sensory deficit up to the level of compression Disruption of bladder/bowel control Lower back aching pain radiating distally
294
What are the investigations for spinal cord compression?
--> MRI spine - T1+T2 weighted
295
What is the treatment for spinal cord compressions?
Surgical laminectomy to relieve the pressure, removal of any mass lesions if possible
296
What is cauda equina?
--> surgical emergency where the nerve roots of the cauda equina at the bottom of the spine as compressed --> The cauda equina is a collection of nerve roots that travel through the spinal canal after the spinal cord terminates around L2/L3
297
What are the causes of Cauda Equina?
→ Herniated disc - most common → tumours - mets → spondylolisthesis - anterior displacement of vertebra out of line with one below → Abscess infection → trauma
298
What is the presentation of Cauda Equina?
→Saddle anaesthesia (loss of sensation in the perineum – around the genitals and anus) → Loss of sensation in the bladder and rectum (not knowing when they are full) → Urinary retention or incontinence → Faecal incontinence → Bilateral sciatica → Bilateral or severe motor weakness in the legs → Reduced anal tone on PR examination
299
What are the investigations for Cauda Equina?
→ medical emergency - immediate neurosurgery referral for lumbar decompression surgery → Emergency MRI scan to confirm
300
What is the treatment for Cauda Equina?
Treatment → Surgical decompression as soon as possible → Immobilise spine → Anti-inflammatory agents → chemotherapy if Mets → antibiotics if an infection is present
301
What are the causes of spinal nerve compression?
lateral lumbar/cervical disc protrusion – secondary to spondylosis (osteoarthritic change in the spine) and/or disc generation Tumours Trauma / mechanical strain
302
What are the clinical features of spinal nerve compression?
--> Radiculopathy - compression of individual nerve root CERVICAL --> pain - Sharp, stabbing pain in affected root distribution, radiating distally from shoulders --> sensory (numbness/paraesthesia) - in dermatomes supplied by the affected nerve roots --> Motor (LMN weakness) - in myotomes supplied by the affected nerve roots - C5 - elbow flexion, C6 - wrist extension, C7 - elbow extension LUMBAR --> Pain - Sharp, stabbing pain in affected root distribution, radiating distally from the lower back (sciatica) --> sensory (numbness/paraesthesia) - in dermatomes supplied by the affected area --> motor - in myotomes supplied by the affected nerve roots - L4 - ankle dorsiflexion, L5 - hallux dorsiflexion, S1 - plantarflexion --> special tests - straight leg raise - painful hip flexion, worsened by ankle dorsiflexion
303
What are the investigations for spinal nerve compression?
--> MRI spine T1+T2 weighted
304
What is the treatment for spinal nerve compression?
Rest +/- analgesics. If pain and more importantly neurological deficit persists: Cervical – anterior cervical discectomy and fusion (ACDF) Lumbar – microdiscectomy
305
What is radiculopathy?
Commonly referred to as a pinched nerve, radiculopathy is injury or damage to nerve roots in the area where they leave the spine. This condition can affect anyone and result from disc degeneration, disc herniation or other trauma.
306
What is Menieres disease?
Ménière’s disease is a long-term inner ear disorder that causes recurrent attacks of vertigo, and symptoms of hearing loss, tinnitus and a feeling of fullness in the ear.
307
What is the typical triad of Menieres disease
Hearing loss Vertigo Tinnitus
308
What is the pathophysiology of Meniere's disease
excessive buildup of endolymph in the labyrinth of the inner ear, causing a higher pressure than normal and disrupting the sensory signals. This increased pressure of the endolymph is called endolymphatic hydrops
309
what is the presentation of Menieres disease?
typical patient 40-50 years old, presenting with unilateral episodes of vertigo, hearing loss and tinnitus --> Vertigo - comes in episodes - last between 20 minutes to several hours, not triggered by movement or posture --> Hearing loss - fluctuates at first, but then becomes more permanent - sensorineural, unilateral and affects low frequencies first --> Tinnitus - initially occurs with episodes of vertigo before eventually becoming more permanent, unilateral --> A sensation of fullness in the ear --> Unexplained falls (“drop attacks”) without loss of consciousness --> Imbalance, which can persist after episodes of vertigo resolve --> Spontaneous nystagmus may be seen during an acute attack - unidirectional
310
What are the investigations for Menieres disease?
--> Diagnosis of Ménière’s disease is clinical, based on the signs and symptoms. It will be made by an ear, nose and throat (ENT) specialist. --> Patients will need an audiology assessment to evaluate hearing loss.
311
What is the management of Meniere's disease?
Management involves: Managing symptoms during an acute attack Prophylactic medication to reduce the frequency of attacks For acute attacks, short-term options for managing symptoms include: Prochlorperazine Antihistamines (e.g., cyclizine, cinnarizine and promethazine) Prophylaxis is with: Betahistine
312
What is myasthenia gravis?
Myasthenia gravis is an autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest typical women under 40 and men over 60
313
What are the causes of myasthenia gravis?
Binding of autoantibodies to acetylcholine receptors in NMJ - blocks postsynaptic receptor - increased activity leads to more receptors blocked - less muscle stimulation with increased activity → Can be inherited
314
What is the presentation of myasthenia gravis?
→ muscle weakness that worsens during physical activity and improves after rest. → Nearly all patients with the condition will experience some form of eye-related symptoms at some point e.g ptosis and diplopia → Proximal muscles are more affected → Weakness may be observed in the small muscles of the hands, as well as the deltoid, triceps, and bulbar muscles, which are responsible for chewing and speaking. → does not typically cause muscle wasting or affect sensation. → Seizures may be a possible complication
315
What are the investigations for myasthenia gravis?
→ Antibody testing - AChR, MuSK and LRP4 → TFT’s → CT/MRI of the thymus to look for thymoma → Edrophonium test - IV neostigmine improves Sx
316
What is the treatment for myasthenia gravis?
→ Symptomatic treatment with reversible acetylcholinesterase inhibitors - pyridostigmine/neostigmine → immunosuppression - prednisolone/azathioprine suppresses the production of antibodies → Monoclonal antibodies - Rituximab/eculizumab - targets B cells and reduces the production of antibodies → Thymectomy → Myasthenic crisis - IVIg + plasmapheresis + Non invasive ventilation
317
What is mononeuropathy?
--> damage or dysfunction of a single peripheral nerve, cranial nerves, spinal nerve etc --> most cause sensory and motor impairment, usually affecting the hands, feet and arms
318
Give some examples of mononeuropathies.
Cubital tunnel syndrome - ulnar nerve neuropathy Carpal tunnel syndrome - median nerve mononeuropathy peroneal nerve dysfunction
319
What are some common causes of mononeuropathies?
--> Nerve compression against a hard surface - compression can cause segmental demyelination --> Entrapment of nerve in narrow anatomical spaces -->Repetitive actions that cause trauma to neuron --> infections, radiation and cold
320
What is the presentation of mononeuropathies?
--> depends on the affected nerve and underlying cause --> Sensory - numbness, pain and tingling --> Motor - weakness, atrophy, loss of coordination
321
How can you treat mononeuropathies?
--> Rest, avoidance or removal of the causative agent --> NSAIDS --> Treat underlying cause! --> immobilising area --> corticosteroids --> decompression
322
What is neurofibramatosis?
--> genetic condition that causes nerve tumours (neuromas) to develop throughout the nervous system --> benign, but causes neurological and structural problems --> two types - NF type 1 and type 2 --> Type 1 more common
323
Which gene is responsible for neurofibromatosis type 1?
NF1 gene on chromosome 17 codes for a protein called neurofibromin - TS protein autosomal dominant inheritance
324
How is the diagnosis of neurofibromatosis type 1 made - criteria
2 of the 7 must be present C – Café-au-lait spots (6 or more) measuring ≥ 5mm in children or ≥ 15mm in adults R – Relative with NF1 A – Axillary or inguinal freckles BB – Bony dysplasia such as Bowing of a long bone or sphenoid wing dysplasia I – Iris hamartomas (Lisch nodules) (2 or more) are yellow-brown spots on the iris N – Neurofibromas (2 or more) or 1 plexiform neurofibroma G – Glioma of the optic nerve
325
What are the investigations of neurofibromatosis type 1
--> clinical criteria --> genetic testing --> X-rays - bone pain and bone lesions --> CT/MRI investigate lesions elsewhere in the body
326
What is the management of neurofibromatosis type 1
There is no treatment of the underlying disease process or to prevent the development of neurofibromas or complications. Management is to control symptoms, monitor the disease and treat complications.
327
What are the complications of neurofibromatosis type 1?
Migraines Epilepsy Renal artery stenosis causing hypertension Learning and behavioural problems (e.g. ADHD) Scoliosis of the spine Vision loss (secondary to optic nerve gliomas) Malignant peripheral nerve sheath tumours A gastrointestinal stromal tumour (a type of sarcoma) Brain tumours Spinal cord tumours with associated neurology (e.g. paraplegia) Increased risk of cancer (e.g. breast cancer) Leukaemia
328
What is the pathophysiology of neurofibromatosis type 2?
The neurofibromatosis type 2 gene is found on chromosome 22. It codes for a protein called merlin, which is a tumour suppressor protein particularly important in Schwann cells. Mutations in this gene lead to the development of schwannomas (benign nerve sheath tumours of the Schwann cells). Inheritance is autosomal dominant.
329
Which neuromas are most associated with neurofibromatosis type 2?
acoustic neuromas - hearing loss, tinnitus, balance problems
330
What is the treatment for neurofibromatosis type 2?
Surgery can be used to resect the tumours, however risk of permanent nerve damage.
331
What is normal pressure hydrocephalus?
--> reversible cause of dementia seen in elderly patients --> thought to be secondary to reduced CSF absorption at the arachnoid villi --> can be secondary to head injury, subarachnoid haemorrhage or meningitis.
332
What is the presentation of normal pressure hydrocephalus?
Classic triad Urinary incontinence dementia and bradyphrenia gait abnormality - similar to Parkinsons symptoms develop over a few months
333
What is the investigation for normal pressure hydrocephalus?
MRI/CT --> Ventriculomegaly/ sulcal enlargement
334
What is the management of normal pressure hydrocephalus?
ventriculoperitoneal shunting
335
How is chronic fatigue syndrome diagnosed?
Diagnosed after at least 3 months of disabling fatigue affecting mental and physical function more than 50% of the time in the absence of other disease which may explain symptoms
336
In which population is chronic fatigue syndrome seen more?
females
337
What is the presentation of chronic fatigue syndrome?
Fatigue is the central feature, other recognised features include --> Sleep problems, such as insomnia, hypersomnia, unrefreshing sleep, a disturbed sleep-wake cycle --> Muscle and/or joint pains --> headaches --> painful lymph nodes without enlargement --> sore throat --> cognitive dysfunction, such as difficulty thinking, inability to concentrate, impairment of short-term memory, and difficulties with word-finding physical or mental exertion makes symptoms worse --> General malaise or 'flu-like' symptoms --> dizziness --> nausea --> palpitations
338
What are the investigations for chronic fatigue syndrome?
NICE guidelines suggest carrying out a large number of screening blood tests to exclude other pathology e.g. FBC, U&E, LFT, glucose, TFT, ESR, CRP, calcium, CK, ferritin, coeliac screening and also urinalysis
339
How is the diagnosis of chronic fatigue syndrome made?
All of these symptoms should be present: Debilitating fatigue that is worsened by activity, is not caused by excessive cognitive, physical, emotional or social exertion, and is not significantly relieved by rest. Post-exertional malaise after activity in which the worsening of symptoms: is often delayed in onset by hours or days is disproportionate to the activity has a prolonged recovery time that may last hours, days, weeks or longer. Unrefreshing sleep or sleep disturbance (or both), which may include: feeling exhausted, feeling flu-like and stiff on waking broken or shallow sleep, altered sleep pattern or hypersomnia. Cognitive difficulties (sometimes described as 'brain fog'), which may include problems finding words or numbers, difficulty in speaking, slowed responsiveness, short-term memory problems, and difficulty concentrating or multitasking.
340
What is the management of chronic fatigue syndrome?
refer to a specialist CFS service if the diagnostic criteria are met and symptoms have persisted for 3 months energy management a self-management strategy that involves a person with ME/CFS managing their activities to stay within their energy limit, with support from a healthcare professional physical activity and exercise do not advise people with ME/CFS to undertake exercise that is not part of a programme overseen by an ME/CFS specialist team should only be recommended if patients 'feel ready to progress their physical activity beyond their current activities of daily living' graded exercise therapy used to be recommended but is now specifically not recommended by NICE cognitive behavioural therapy NICE stress this is 'supportive' rather than curative for CFS
341
What is narcolepsy?
--> low levels of orexin (hypocretin) a protein which is responsible for controlling appetite and sleep patterns --> early onset REM sleep --> associated with HLA-DR2
342
What are the features of narcolepsy?
typical onset in teenage years hypersomnolence cataplexy (sudden loss of muscle tone often triggered by emotion) sleep paralysis vivid hallucinations on going to sleep or waking up
343
What are the investigations for narcolepsy?
multiple sleep latency EEG
344
what is the management of narcolepsy?
daytime stimulants - modafinil nighttime sodium oxybate
345
What is diabetic neuropathy?
--> a type of peripheral neuropathy typically leading to sensory loss and not motor loss --> complication of diabetes
346
What is the presentation of diabetic neuropathy?
--> sensory loss and not motor loss --> sensory loss in glove and stocking distribution --> lower legs affected first
347
What is the management of diabetic neuropathy?
--> managed in the same way to neuropathic pain first-line treatment: amitriptyline, duloxetine, gabapentin or pregabalin if the first-line drug treatment does not work try one of the other 3 drugs tramadol may be used as 'rescue therapy' for exacerbations of neuropathic pain topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia) pain management clinics may be useful in patients with resistant problems
348
At what level does the spinal cord end?
L1 - splits into the cauda equina
349
What are the two ascending tracts in the spinal cord?
Dorsal column spinothalamic tract
350
Describe the dorsal column in the spinal cord
the posterior section of the spinal cord carries information about fine touch, vibration, proprioception decussates just before it reaches the medulla - remains ipsilateral
351
Describe the spinothalamic tract in the spinal cord
the anterior section of the spinal cord information regarding pain and temperature fibres decussate immediately as then enter the cord ascend contralaterally
352
What is the main descending tract in the spinal cord?
Corticospinal tract
353
Describe the corticospinal tract in the spinal cord
--> carries motor information from the frontal lobe to skeletal muscles --> immediately decussate when entering the spinal cord --> Fibres travel contralaterally
354
What is the presentation when there is a complete transection of the spinal cord?
interruption of all ascending and descending tracts bilaterally, resulting in bilateral loss of motor function, and complete loss of all modes of sensation below the level of the lesion.
355
What is brown-sequard syndrome?
lateral hemisection of the spinal cord
356
What is the presentation of brown-sequard syndrome?
ipsilateral weakness below the lesion- corticospinal tract decussates near the medulla ipsilateral loss of proprioception and vibration sensation, fine touch - dorsal columns do not immediately decussate contralateral loss of pain and temperature sensation - spinothalamic tract decussates immediately
357
What is anterior cord syndrome?
front of the spinal cord is damaged and the posterior aspect is preserved
358
What is the presentation of anterior cord syndrome?
--> Bilateral loss of pain and temperature sensation - spinothalamic in anterior portion damaged --> Bilateral spastic paralysis and UMN signs - corticospinal tracts can also be damaged --> dorsal column intact so fine touch, proprioception and vibration will be intact
359
What is carpal tunnel syndrome?
Carpal tunnel syndrome is caused by compression of the median nerve as it travels through the carpal tunnel in the wrist, causing pain and numbness in the median nerve distribution on the hand.
360
Why can the median nerve become compressed in carpal tunnel syndrome?
Swelling of the contents (e.g., swelling of the tendon sheaths due to repetitive strain) Narrowing of the tunnel
361
What is the median nerve responsible for in the hand?
sensory innervation of the palmar aspects and full fingertips of the thumb, index and middle finger and the lateral half of the ring finger motor function of thenar muscles at the base of the thumb - Abductor pollicis brevis (thumb abduction) Opponens pollicis (thumb opposition – reaching across the palm to touch the tips of the fingers) Flexor pollicis brevis (thumb flexion
362
What are the risk factors for carpal tunnel syndrome
idiopathic Repetitive strain Obesity Perimenopause Rheumatoid arthritis Diabetes Acromegaly Hypothyroidism
363
What is the presentation of carpal tunnel syndrome?
gradual onset, intermittent, worse at night Numbness Paraesthesia (pins and needles or tingling) Burning sensation Pain motor symptoms - thenar muscles affected Weakness of thumb movements Weakness of grip strength Difficulty with fine movements involving the thumb Wasting of the thenar muscles (muscle atrophy)
364
What are two special tests for carpal tunnel syndrome?
Phalens Tinels
365
What are the investigations for carpal tunnel syndrome?
Carpal tunnel questionare Nerve conduction studies
366
What is the management for carpal tunnel syndrome?
Rest and altered activities Wrist splints that maintain a neutral position of the wrist can be worn at night (for a minimum of 4 weeks) Steroid injections Surgery - flexor retinaculum cut to release the pressure on the median nerve
367
What is peroneal neuropathy?
--> Common peroneal nerve compressed against the head of the fibula
368
What is the presentation of peroneal neuropathy?
Foot drop - ankle dorsiflexion deficit, ankle eversion also affected sensory deficit over dorsal foot
369
What is ulnar neuropathy?
--> entrapment of the ulnar nerve at the cubital tunnel of the elbow
370
What is the presentation of ulnar neuropathy?
Weakness/wasting of muscles supplied by the ulnar nerve such as adductor pollicis in the thumb
371
What is the treatment of ulnar neuropathy?
Avoid pressure splinting
372
What are the potential causes of a brain abscess
Extension of sepsis from the middle ear or sinuses trauma Surgery to scalp penetrating head injuries embolic events from endocarditis
373
What is the presentation of someone with a brain abcess?
depends on the site --> headache often dull, persistent --> fever may be absent and usually not the swinging pyrexia seen with abscesses at other sites --> focal neurology e.g. oculomotor nerve palsy or abducens nerve palsy secondary to raised intracranial pressure --> Other features consistent with raised intracranial pressure nausea papilloedema seizures
374
What are the investigations for brain abscesses?
CT head
375
What is the management of brain abscess?
Surgery: Craniotomy is performed and the abscess cavity debrided - the abscess may reform because the head is closed following abscess drainage. IV antibiotics: IV 3rd-generation cephalosporin + metronidazole Intracranial pressure management: e.g. dexamethasone
376
What are the causes of delirium?
Causes: HE IS NOT MAAD Hypoxia - resp failure, MI, PE Endocrine - cushing's, thyroid, glucose Infection - pneumonia, UTI Stroke - ^ICP, head trauma Nutrition - thiamine/B12 def Others - pain, lack of sleep Theatre - anaesthetics Metabolic - electrolytes Abdominal - urine retention Alcohol - intox + withdrawal Drugs - BZD, opioids
377
What are the causes of falls in the elderly?
General --> Mechanical (e.g. poor footwear/visual impairment)/ Polypharmacy Cardiovascular --> Arrhythmias/ Orthostatic hypotension/ Bradycardia/ Valvular heart disease Neurological --> Stroke/ Peripheral neuropathy/ gait abnormalities Genitourinary --> Incontinence/ Urinary tract infection Endocrine --> Hypoglycaemia Musculoskeletal --> Arthritis/ Disuse atrophy ENT --> Benign paroxysmal positional vertigo Ear wax
378
What are the investigations for falls in the elderly?
Bedside --> Vital signs (BP/HR/RR/SpO2/Temperature) - Sepsis/ Bradycardia --> Lying and standing blood pressure - Orthostatic hypotension --> Urine dipstick - Infection/ Rhabdomyolysis (+++ blood) --> ECG -Bradycardia/ Arrhythmias Cognitive screening (e.g. AMT) --> Cognitive impairment Blood glucose --> Hypoglycaemia secondary to poor oral intake Bloods--> Full blood count - Anaemia/ Infection (raised white cells) --> Urea and electrolytes - Dehydration/Electrolyte abnormalities/ Rhabdomyolysis --> Liver function tests - Chronic alcohol use --> Bone profile - Calcium abnormalities in malignancy/ Over-supplementation of calcium --> Imaging Chest X-ray - Pneumonia --> CT head- Chronic or acute subdural Stroke --> Echo - Valvular heart disease (e.g aortic stenosis) --> Specialist - Tilt table test Dix-Hallpike test - Benign paroxysmal positional vertigo --> Cardiac monitoring (e.g. 48hr tape) If no symptoms during the monitoring episode in the hospital
379
What is the management of falls in the elderly?
1 Gait --> Physiotherapy 2 Visual problems --> Eye test and ensure wears glasses 3 Hearing Difficulties --> Remove earwax/ Hearing assessment 4 Medications review --> Reduce unnecessary medication 5 Alcohol intake --> Alcohol cessation advice Alcohol service referral 6 Cognitive impairment --> Referral to a psychiatric team 7 Postural hypotension --> Review medication/ Improve hydration 8 Continence --> Treat or rule out infections Continence assessment 9 Footwear --> Ensure good-fitting footwear 10 Environmental hazards --> Turn on lights Take up rugs
380
Name some medications that can cause postural hypotension
Nitrates Diuretics Anticholinergic medications Antidepressants Beta-blockers L-Dopa Angiotensin-converting enzyme inhibitors - (ACE) inhibitors
381
Name some medications that are associated with falls due to mechanisms not associated with postural hypotension
Benzodiazepines Antipsychotics Opiates Anticonvulsants Codeine Digoxin Other sedative agents
382
Which scoring questionnaire can be used to assess frailty?
PRISMA-7
383
What is Osteoporosis
Osteoporosis is a condition where there is a reduction in bone mineral density
384
What is osteopenia?
refers to a less severe reduction in bone density than osteoporosis. Reduced bone density makes bone less strong and more prone to fractures
385
What are the risk factors for osteoporosis?
Older age Female Reduced mobility and activity Low BMI (<18.5 kg/m2) Rheumatoid arthritis Alcohol and smoking Long term corticosteroids. NICE suggest the risk increases significantly with the equivalent of more than 7.5mg of prednisolone per day for more than 3 months) Other medications such as SSRIs, PPIs, anti-epileptics and anti-oestrogens
386
in which group of women should osteoporosis be considered?
Post-menopausal women are a key group where osteoporosis should be considered. Oestrogen is protective against osteoporosis. Unless they are on HRT postmenopausal women have less oestrogen. They also tend to be older and often have other risk factors for osteoporosis.
387
What are the investigations for osteoporosis?
--> FRAX score - the risk of fracture in 10 years, gives results as a percentage 10-year probability of a major osteoporotic fracture and Hip fracture. Age, BMI, co-morbidities, smoking, alcohol and family history. You can enter a result for bone mineral density (from a DEXA scan) --> Dexa scan - done at hip, measures BMD, Z score corrected to patients age/ T-score - BMD of a healthy young person - >-1 = normal/ -1 - -2.5 = osteopenia/ <-2.5 = osteoporosis/ <-2.5 + # = severe osteoporosis
388
What is the management for osteoporosis?
--> Calcichew D3 - calcium and vitamin D (colecalciferol) supplementation + Bisphosphonates - They work by interfering with osteoclasts and reducing their activity, preventing the reabsorption of bone (Alendronate/Risedronate/ zoledronic acid) --> Alternatives --> Denosumab monoclonal antibody that works by blocking the activity of osteoclasts. --> Strontium ranelate is a similar element to calcium that stimulates osteoblasts and blocks osteoclasts but increases the risk of DVT, PE and myocardial infarction. --> Raloxifene is used as secondary prevention only. It is a selective oestrogen receptor modulator that stimulates oestrogen receptors on bone but blocks them in the breasts and uterus. --> Hormone replacement therapy should be considered in women that go through menopause early.
389
What are the side effects of bisphosphonates and how should they be taken?
Reflux and oesophageal erosions. Oral bisphosphonates are taken on an empty stomach sitting upright for 30 minutes before moving or eating to prevent this. Atypical fractures (e.g. atypical femoral fractures) Osteonecrosis of the jaw Osteonecrosis of the external auditory canal
390
How is constipation defined?
It may be defined as defecation that is unsatisfactory because of infrequent stools (< 3 times weekly), difficult stool passage (with straining or discomfort), or seemingly incomplete defecation
391
What are the complications of constipation?
overflow diarrhoea acute urinary retention haemorrhoids
392
Which diagnostic criteria can be used for constipation?
The Rome IV diagnostic criteria for constipation include spontaneous bowel movements occurring fewer than three times a week.
393
How is chronic constipation defined?
Chronic constipation usually describes symptoms which are present for at least three months.
394
What are the causes of constipation?
Functional (primary or idiopathic) constipation is chronic constipation without a known cause. Secondary (organic) constipation is constipation caused by a drug or underlying medical condition.
395
What should the assessment of someone with constipation include?
Identification of red flag symptoms or signs that may suggest a serious underlying cause, such as colorectal cancer. Exploration of the person’s understanding of constipation and their normal pattern of defecation including the frequency and consistency of stools, symptoms of faecal impaction and/or incontinence. Assessment of associated rectal, abdominal, or urinary symptoms. The severity and impact of symptoms on daily life and functioning. Any risk factors or possible secondary causes. Any self-help measures or drug treatments tried. Abdominal and rectal examination.
396
what is benign paroxysmal positional vertigo?
Benign paroxysmal positional vertigo (BPPV) is a common cause of recurrent episodes of vertigo triggered by head movement. It is a peripheral cause of vertigo, meaning the problem is located in the inner ear rather than the brain. It is more common in older adults.
397
what is the pathophysiology of benign paroxysmal positional vertigo?
BPPV is caused by crystals of calcium carbonate called otoconia that become displaced into the semicircular canals. This occurs most often in the posterior semicircular canal. They may be displaced by a viral infection, head trauma, ageing or without a clear cause. The crystals disrupt the normal flow of endolymph through the canals, confusing the vestibular system. Head movement creates the flow of endolymph in the canals, triggering episodes of vertigo.
398
What are the causes of benign paroxysmal positional vertigo?
-->Head injury -->Vestibular neuronitis (post-viral illness) -->Labyrinthitis (due to age-related degeneration of the labyrinth) --> Complications of mastoid/stapes surgery
399
What are the risk factors of benign paroxysmal positional vertigo?
Older age (onset common between 40 to 60 years old). Female sex (women are twice as likely to have BPPV compared to men) Meniere’s disease (usually diagnosed alongside BPPV in 30% of cases) Patients with migraines and/or anxiety disorders
400
What is the presentation of benign paroxysmal positional vertigo?
Typical symptoms of BPPV include: Brief episodes of vertigo usually lasting 30 seconds to 1 minute Symptoms provoked by head movements such as rolling over in bed, gazing upwards (e.g. when placing an object on a shelf), bending forward (e.g. when tying shoe laces, sitting down) Less common symptoms include: Nausea Light-headedness, imbalance (as a result, patients may present with a fall – hence, it is crucial to consider vestibular dysfunction; see the Geeky Medics guide to the assessment of falls) Dix-Hallpike test positive - rotational vertigo and nystagmus
401
What are the investigations for benign paroxysmal positional vertigo?
--> Dix-Hallpipe manouvre
402
What are the differentials for benign paroxysmal positional vertigo?
Persistent vertigo: indicative of Meniere’s disease Tinnitus, hearing loss or aural fullness: indicative of Meniere’s disease, labyrinthitis Long and gradual onset, viral prodrome: indicative of vestibular neuronitis, labyrinthitis Visual, speech, motor or sensory loss: indicative of a CNS lesion Vertical/down-beating nystagmus: indicative of a CNS lesion
403
What is the management for benign paroxysmal positional vertigo?
--> BPPV is often a self-limiting condition, and symptoms may subside within 6 months of onset. Patients should be advised to: Avoid positions that may provoke vertigo symptoms and Counsel that symptoms may re-occur. One study identified a 36% symptom recurrence rate within 48 months of onset. --> If sx persists then vestibular rehabilitation- Epley manoeuvre - reposition the displaced otoconial particles back into the utricle/ Brandt-Daroff exercises
404
What are the two types of urinary incontinence?
Urge incontinence Stress incontinence
405
What is urge incontinence?
Urge incontinence is caused by overactivity of the detrusor muscle of the bladder. Urge incontinence is also known as overactive bladder. The typical description is of suddenly feeling the urge to pass urine, having to rush to the bathroom and not arriving before urination occurs
406
What is stress incontinence?
Stress incontinence is due to the weakness of the pelvic floor and sphincter muscles. This allows urine to leak at times of increased pressure on the bladder. The typical description of stress incontinence is urinary leakage when laughing, coughing or being surprised.
407
What is overflow incontinence?
Chronic urinary retention due to obstruction to the outflow of urine. Chronic urinary retention results in an overflow of urine, and incontinence occurs without the urge to pass urine. It can occur with anticholinergic medications, fibroids, pelvic tumours and neurological conditions such as multiple sclerosis, diabetic neuropathy and spinal cord injuries.
408
What are the risk factors for urinary incontinence?
Increased age Postmenopausal status Increase BMI Previous pregnancies and vaginal deliveries Pelvic organ prolapse Pelvic floor surgery Neurological conditions, such as multiple sclerosis Cognitive impairment and dementia
409
What are the investigations for urinary incontinence?
A bladder diary should be completed, tracking fluid intake and episodes of urination and incontinence over at least three days. There should be a mix of work and leisure days. Urine dipstick testing should be performed to assess for infection, microscopic haematuria and other pathology. Post-void residual bladder volume should be measured using a bladder scan to assess for incomplete emptying. Urodynamic testing can be used to investigate patients with urge incontinence not responding to first-line medical treatments, difficulties urinating, urinary retention, previous surgery or an unclear diagnosis. It is not always required where the diagnosis is possible based on the history and examination.
410
What is the management of stress incontinence?
Avoiding caffeine, diuretics and overfilling of the bladder Avoid excessive or restricted fluid intake Weight loss (if appropriate) Supervised pelvic floor exercises for at least three months before considering surgery Surgery Duloxetine is an SNRI antidepressant used second line where surgery is less preferred
411
what is the management of urge incontinence?
Bladder retraining (gradually increasing the time between voiding) for at least six weeks is first-line Anticholinergic medication, for example, oxybutynin, tolterodine and solifenacin SE dry mouth, dry eyes, urinary retention, constipation and postural hypotension and worsening dementia Mirabegron is an alternative to anticholinergic medications Invasive procedures where medical treatment fails
412
What is malnutrition?
a sudden or chronic decrease in the intake of sufficient nutrition to support the body’s requirements for growth, healing, and maintenance of life. Malnutrition can be acute or chronic (longer than 3 months)
413
What are the four main reasons why someone may be malnourished?
Inadequate amounts of nutrients (e.g. poor variety in diet) Difficulty absorbing nutrients (e.g. gastrointestinal dysfunction such as coeliac disease) Increased nutritional demands (e.g. post-surgery for healing or increased metabolic demands due to illness and certain drugs)
414
What are the risk factors for malnutrition?
--> Those with chronic illnesses --> Living in supported accommodations --> Excessive alcohol intake --> Being hospitalised for extended periods of time --> Problems with dentition, taste or smell --> Polypharmacy --> Social isolation and loneliness --> Mental health issues including grief, anxiety and -------> depression --> Cognitive issues including confusion
415
What is the presentation of malnutrition?
High susceptibility or long durations of infections Slow or poor wound healing Altered vital signs including bradycardia, hypotension, and hypothermia Depleted subcutaneous fat stores Low skeletal muscle mass
416
What investigations should be carried out for malnutrition?
--> Hx - weight, meals, protein, hydration --> Weight, BMI, muscle mass and subcutaneous fat stores
417
What is the management of malnutrition?
--> Dieticians lead management --> If a reversible cause is found e.g infection treat it --> Oral nutritional support --> Parenteral nutrition for those unable to swallow or intestinal failure
418
What is refeeding syndrome?
--> caused by the rapid reintroduction of normal nutrition in patients who are chronically malnourished --> In chronic malnutrition patients their intracellular stores of electrolytes such as potassium and phosphate are depleted --> Sudden normal nutrition leads to a sudden shift of these electrolytes from extracellular to intracellular driven by a large insulin response --> Sudden drop in extracellular electrolytes leading to hypokalemia and hypophosphataemia --> can lead to arrhythmias and seizures
419
What are the complications of malnutrition?
Impaired immunity (increased risk of infections) Poor wound healing Growth restriction in children Unintentional weight loss, specifically the loss of muscle mass Multi-organ failure Death
420
What is chronic heart failure?
clinical features of impaired heart function, specifically the function of the left ventricle to pump blood out of the heart and around the body.
421
What is the pathophysiology of chronic heart failure?
--> impaired left ventricular function - chronic backlog of blood to the left ventricle - left atrium/pulmonary veins and lungs experience increased volume and pressure - leads to pulmonary oedema --> Heart failure with reduced ejection fraction - <50% --> Heart failure with preserved ejection fraction - >50% - issue with ventricles filling with blood - diastolic dysfunction
422
What are the causes of chronic heart failure?
Ischaemic heart disease Valvular heart disease (commonly aortic stenosis) Hypertension Arrhythmias (commonly atrial fibrillation) Cardiomyopathy
423
What is the presentation of someone with chronic heart failure?
Breathlessness, worsened by exertion Cough, which may produce frothy white/pink sputum Orthopnoea, which is breathlessness when lying flat, relieved by sitting or standing (ask how many pillows they use) Paroxysmal nocturnal dyspnoea Peripheral oedema Fatigue
424
What signs would there be on clinical examination for chronic heart failure?
Tachycardia (raised heart rate) Tachypnoea (raised respiratory rate) Hypertension Murmurs on auscultation indicating valvular heart disease 3rd heart sound on auscultation Bilateral basal crackles (sounding “wet”) on auscultation of the lungs, indicating pulmonary oedema Raised jugular venous pressure (JVP), caused by a backlog on the right side of the heart, leading to an engorged internal jugular vein in the neck Peripheral oedema of the ankles, legs and sacrum
425
What are the investigations for chronic heart failure?
--> Clinical assessment - Hx and examination --> NT-proBNP bloods --> ECG --> Echocardiogram --> Bloods - to look for anaemia, renal function, thyroid function, liver function, lipids and diabetes --> chest X-ray and lung function tests to exclude lung pathology
426
What are the five principles of management for chronic heart failure?
R – Refer to cardiology A – Advise them about the condition M – Medical treatment P – Procedural or surgical interventions S – Specialist heart failures MDT input, such as the heart failure specialist nurses, for advice and support
427
What is the medical treatment for chronic heart failure?
A – ACE inhibitor (e.g., ramipril) titrated as high as tolerated B – Beta blocker (e.g., bisoprolol) titrated as high as tolerated A – Aldosterone antagonist when symptoms are not controlled with A and B (e.g., spironolactone or eplerenone) L – Loop diuretics (e.g., furosemide or bumetanide) additional specialist treatments - SGLT2 inhibitor (e.g., dapagliflozin) Sacubitril with valsartan (brand name Entresto) Ivabradine Hydralazine with a nitrate Digoxin
428
What is the procedural and surgical interventions for chronic heart failure?
--> can treat underlying valvular heart disease --> Implantable cardioverter defibrillators - for patients who have had ventricular tachycardia or V fib before --> Cardiac resynchronization therapy CRT - severe heart failure with EF < 35%, involves bi-ventricular pacemakers - leads to the right atrium and both ventricles - aim to synchronise the contractions --> heart transplant in severe disease
429
What is acute heart failure?
AHF involves the acute failure of the heart to pump blood to meet the body’s demand
430
What is the pathophysiology of acute heart failure?
Congestion in the pulmonary or systemic circulation. Pulmonary oedema develops when the left ventricle is unable to empty, which increases the hydrostatic pressure in pulmonary vasculature leading to pulmonary oedema and hypoxia. These patients are ‘WET’. Hypoperfusion of vital organs as the cardiac output is reduced. These patients are ‘COLD’. 50% of patients will show signs of congestion without signs of hypoperfusion (WET-WARM). 45% of patients will show signs of congestion with signs of hypoperfusion (WET-COLD). 5% of patients will show no signs of congestion (DRY-WARM or DRY-COLD).
431
What are the causes of acute heart failure?
Causes of new-onset AHF include: Acute myocardial dysfunction (e.g. ischaemia due to myocardial infarction) Acute valve dysfunction Arrhythmias Causes of acute decompensation of CHF include: Infection Acute myocardial dysfunction (e.g. ischaemia due to myocardial infarction) Uncontrolled hypertension Arrhythmias Worsening chronic valve disease Non-adherence with drugs/diet Change in drug regimen Withdrawal/reduction of heart failure medications inappropriately Initiation/increase of rate-control medications inappropriately Other medications: steroids, non-steroidal anti-inflammatories, pioglitazones
432
What is the presentation of someone with acute heart failure?
Acute LVF causes a type 1 respiratory failure (low oxygen without an increased carbon dioxide). Symptoms include: Shortness of breath Looking and feeling unwell Cough with frothy white or pink sputum Signs on examination include: Raised respiratory rate Reduced oxygen saturations Tachycardia (fast heart rate) 3rd heart sound Bilateral basal crackles (sounding “wet”) on auscultation of the lungs Hypotension in severe cases (cardiogenic shock) There may also be signs and symptoms related to the underlying cause, for example: Chest pain in acute coronary syndrome Fever in sepsis Palpitations with arrhythmias If they also have right-sided heart failure, you could find: Raised jugular venous pressure (JVP), caused by a backlog on the right side of the heart, leading to an engorged internal jugular vein in the neck Peripheral oedema of the ankles, legs and sacrum
433
What are the investigations for someone with acute heart failure?
--> Clinical assessment (history and examination, starting with an ABCDE approach in any acutely unwell patient) --> ECG to look for ischaemia and arrhythmias --> Blood for anaemia, infection, kidney function, BNP - sensitive but not specific - shows overload of heart , and consider troponin if suspecting myocardial --> infarction --> Arterial blood gas (ABG) --> Chest x-ray - Alveolar oedema (bat wing shadowing) , Kerley B lines (interstitial oedema) , cardiomegaly, dilated upper lobe vessels, pleural effusions - loss of costophrenic angle --> Echocardiogram - structural abnormalities and ejection fraction
434
What is the management of acute heart failure?
S – Sit-up - fluid sinks to lung bases O – Oxygen - if stats less than 95% D – Diuretics - IV furosemide I – Intravenous fluids should be stopped U – Underlying causes need to be identified and treated (e.g., myocardial infarction) M – Monitor fluid balance Severe cases may require (guided by an experienced specialist): Intravenous opiates, such as morphine, which act as vasodilators Intravenous nitrates act as vasodilators and may be considered in severe hypertension or acute coronary syndrome Inotropes, such as dobutamine, to improve cardiac output Vasopressors, such as noradrenalin, to improve blood pressure Non‑invasive ventilation Invasive ventilation (involving intubation and sedation)
435
What causes pressure ulcers in patients?
Pressure ulcers develop in patients who are unable to move parts of their body due to illness, paralysis or advancing age. They typically develop over bony prominences such as the sacrum or heel.
436
What factors predispose someone of developing pressure ulcers?
malnourishment incontinence lack of mobility pain (leads to a reduction in mobility)
437
Which scoring system screens patients who are at risk of developing pressure ulcers?
Waterlow score
438
Describe the grades for pressure ulcers
Grade 1--> Non-blanch-able erythema of intact skin. Discolouration of the skin, warmth, oedema, induration or hardness may also be used as indicators, particularly on individuals with darker skin Grade 2--> Partial thickness skin loss involving epidermis or dermis, or both. The ulcer is superficial and presents clinically as an abrasion or blister Grade 3 Full-thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia. Grade 4 Extensive destruction, tissue necrosis, or damage to muscle, bone or supporting structures with or without full-thickness skin loss
439
What is the management of pressure ulcers?
--> A moist wound environment encourages ulcer healing. Hydrocolloid dressings and hydrogels may help facilitate this. The use of soap should be discouraged to avoid drying the wound --> Swabs should not be done routinely as the vast majority of pressure ulcers are colonised with bacteria. --> The decision to use systemic antibiotics should be taken on a clinical basis (e.g. Evidence of surrounding cellulitis) --> consider referral to the tissue viability nurse surgical debridement may be beneficial for selected wounds
440
What is the pathological feature of lewy body dementia?
Presence of lewy bodies in the susbtantia nigra, paralimbic and neocortical areas
441
lewy bodies are also seen in which type of dementia?
up to 40% of patients with Alzheimer's have Lewy bodies.
442
What is the presentation of lewy body dementia?
-progressive cognitive impairment --> typically occurs before parkinsonism, but usually both features occur within a year of each other. This is in contrast to Parkinson's disease, where the motor symptoms typically present at least one year before cognitive symptoms --> cognition may be fluctuating, in contrast to other forms of dementia --> in contrast to Alzheimer's, early impairments in attention and executive function rather than just memory loss -parkinsonism -visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen
443
how is the diagnosis of Lewy body dementia made?
--> usually clinical --> single-photon emission computed tomography (SPECT) is increasingly used. It is currently commercially known as a DaTscan. Dopaminergic iodine-123-radiolabelled 2-carbomethoxy-3-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (123-I FP-CIT) is used as the radioisotope. The sensitivity of SPECT in diagnosing Lewy body dementia is around 90% with a specificity of 100%
444
What is the management of Lewy body dementia?
--> Both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer's. --> neuroleptics should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism. Questions may give a history of a patient who has deteriorated following the introduction of an antipsychotic agent
445
Which drug should not be given to a patient with Lewy body dementia?
neuroleptics - antipsychotics as patients can develop irreversible parkinsonism
446
What is the presentation of frontotemporal dementia?
--> personality change --> impaired social conduct --> hyperorality --> disinhibtion --> increased appetite --> perseveration behaviours
447
What are the macroscopic and microscopic changes seen in frontotemporal dementia?
--> atrophy of the frontal and temporal lobes - macroscopic --> micrscopic --> spherical aggregations of Tau protein
448
What is the presentation of frontotemporal dementia?
Signs and Symptoms ● Onset tends to be insidious and progressive ● Present with 3 main symptoms: ○ Behavioural issues, e.g. loss of inhibition/empathy, compulsive behaviours, difficulty planning ○ Progressive aphasia, e.g. slow, difficult speech, grammatical errors ○ Semantic dementia, e.g. loss of vocabulary, problems understanding
449
What are the investigations for frontotemporal dementria?
Bloods - B12, TFTs, U&Es (?other causes) ● FBC and LFTs for suspected encephalopathy ● MMSE ● MRI - frontal/temporal atrophy