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Medicine year 3- EOCP > Neurology- core conditions 3 > Flashcards

Neurology- core conditions 3 Flashcards

1
Q

Peripheral nervous system (PNS) disease: sensory symptom distribution

A

The sensory symptoms are symmetrical, or in the territory of a sensory dermatome or the cutaneous distribution of a peripheral nerve.

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2
Q

Lower motor neurone lesions

A

Atrophy, fasciculations, reduced tone, diminished reflexes

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3
Q

Ascending peripheral neuropathy

A
  • Symptoms started distally and progressed proximally
  • LMN signs
  • Affecting motor and sensory systems
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4
Q

Guilan Barre syndrome

A
  • Acute demyelinating polyneuropathy
  • May be post infectious- camylobacter gastroenteritis, viral
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5
Q

Upper motor neurone lesion

A
  • No atrophy or fasciculations
  • Spastic tone
  • Brisk reflexes
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6
Q

Cervical cord compression

A
  • Bilateral UMN signs (brisk reflexes and increased tone) below the level of the lesion
  • Slowly progressive spastic parapesis
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7
Q

Damage to the different cervical roots

A
  • C5 root- upper lateral arm, never below the elbow
  • C6 root- lower lateral arm, into thumb if pain goes through the hand
  • C7 root- deep pain in triceps area. Front and back of forearm and into the middle finger especially
  • C8 root- pain in the medial forearm and into the two medial finger
  • T1 root- deep pain in the axilla and shoulder with some radiation down the inside of the arm
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8
Q

Cervical spondylosis with myelopathy

A
  • Osteoarthritis is a risk factor
  • Nerve root problem with compression of the cord
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9
Q

Cerebellar signs (DANISH)

A
  • Dysdiadochokinesis
  • Ataxia
  • Nystagmus
  • Intention tremor
  • Slurred speech
  • Hypotonia
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10
Q

Myopathic neurological defect

A
  • Proximal, fatigable weakness
  • Minimal atrophy
  • No fasciculations
  • Normal/reduced tone
  • Normal reflexes
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11
Q

Myasthenia gravis

A
  • Disorder of neuromuscular transmission
  • Positive anti-AChR antibodies
  • Abnormal EMG
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12
Q

Cranial nerve abnormalities

A
  • CNIII (oculomotor)- right eye down and out (MR, IR, SR, IO), Mydriasis (pupillary constrictor), Ptosis (levator palpebrae superioris)
  • VI (abducens)- diplopia on right gaze (LR)
  • Ophthalmic division of V (trigeminal)- altered sensation to right forehead.
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13
Q

Cavernous sinus thrombosis

A
  • Central dural sinus
  • Receives venous drainage from facial veins
  • Structures passing through include ICA and several cranial nerves
  • Infections from face, nose, and tonsils can easily spread here
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14
Q

Neurological red flags in back pain

A
  • Sphincter or gait disturbance
  • Saddle anaesthesia
  • Progressive motor loss
  • Bilateral sciatica
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15
Q

Other red flags in pack pain

A
  • Non-mechanical pain (at rest)
  • Fever or weight loss
  • Age <20 or >55
  • Thoracic pain
  • Previous history of cancer
  • HIV
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16
Q

Dysphonia

A

A hoarse voice. Occurs when there is altered airflow through the larynx which could be due to a pathology at the level of the vocal cords or their neuromuscular control

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17
Q

The larynx

A

Protects the airway, Phonation, regulated air flow into the lungs. It’s a cartilaginous skeleton held together by ligaments and membranes

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18
Q

Physiology of phonation

A
  • Power supply- lungs/ diaphragm/ muscles of respiration to produce air flow
  • Oscillator- focal folds to cause the air being expelled to vibrate
  • Articulator- pharynx, nasal cavity, oral cavity to resonate the sounds to produce speech
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19
Q

Vocal cord function

A
  • During phonation air is expelled between adducted vocal cords resulting in their vibration.
  • The intrinsic muscles of the larynx alter the shape, tension and position of the cords altering pitch and character.

All the muscle of the larynx are supplied by the recurrent laryngeal nerve except the cricothyroid muscle

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20
Q

Red flag symptoms for dysphonia

A
  • Persistent sore throat/odynophagia
  • Persistent dysphagia
  • Persistent unilateral otolgia (ear pain)
  • Persistent cough/ shortness of breath or haemoptyosis
  • Weight loss
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21
Q

Infective/ inflammatory causes of dysphonia

A
  • Acute/chronic laryngitis
  • Epiglottitis
  • Angioedema
  • Burns
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22
Q

Neurological causes of dysphonia

A
  • Parkinsons disease
  • Myasthenia Gravis
  • Motor neurone disease
  • Spasmodic dysphonia
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23
Q

Neoplastic causes of dysphonia

A
  • Congenital- unilateral/bilateral vocal cord palsy, laryngeal web
  • Iatrogenic/trauma- incubation, past thyroid/ cardiothoracic/ cervical surgery. Blunt/penetrating neck trauma
  • Functional- muscle tension/ vocal fatigue, anxiety, depression
  • Systemic- vasculitis, amyloidosis, SLE, rheumatoid arthritis
24
Q

The most common causes of dysphonia is order of prevailence are

A

Laryngitis, Functional, Malignancy

25
Q

Causes of dysphonia- acute laryngitis

A
  • Usually viral and self limiting within 1-2 weeks.
  • No sinister features
  • Treatment: voice rest, vocal hygiene (plenty of fluids, steam inhalation, avoid shouting/whispering)
26
Q

Causes of dysphonia- chronic laryngitis

A
  • Secondary to voice abuse, irritant exposure (tobacco, allergens), reflux, medications (inhaled corticosteroids)
  • Linked to development of nodules, granulomas, polyps
  • Treatment: removal of irritants, vocal hygiene
27
Q

Causes of dysphonia- Benign vocal cord lesions

A
  • Nodules, cysts, polyps, papillomas
  • Present with dysphonia often with history of irritant exposure, excess voice abuse.
  • Human papilloma virus may cause recurrent laryngeal papillomas in the younger population.
  • Nodules are managed with voice hygiene and speech therapy is key. Cyst/polyps are managed by surgical excision (and biopsy to exclude malignancy).
28
Q

Causes of dysphonia- Laryngeal malignancy

A
  • Present with persistent dysphonia; if present early to doctor will often allow curative treatment.
  • Late presentation may be with upper airway obstruction-stridor, SOB, airway emergency
  • Mostly squamous cell carcinomas
  • More common in males (5:1)
  • Median age 6-7th decade, rare under 40 years
  • Associated with smoking and alcohol abuse
  • Good survival outcomes in early stage disease
  • Treatment-laser excision, radiotherapy, chemotherapy, surgery-partial/total laryngectomy
29
Q

Causes of dysphonia- vocal cord paralysis

A
  • Incomplete cord closure will result in dysphonia and may also result in aspiration.
  • Unilateral palsy is the most common and the nerve damage can be anywhere along the course of the vagus nerve from the brainstem to the neck.
  • The affected cord lies in a medialised position (paramedian) and therefore the contralateral working vocal cord needs to stretch beyond the midline to give good voice production. This leads to a weak voice.
  • Vocal cord medialisation procedures are undertaken to allow the contralateral side to meet the affected side more efficiently.
30
Q

Causes of vocal cord paralysis

A
  • Idiopathic- 75% of cases
  • Neoplasia- lung (usually left), thyroid
  • Iatrogenic- recent surgery on neck, thorax, skull base and cervical spine
  • Management- if no identifiable cause, there will be CT from skull base to diaphragm to identify pathology along the vagus nerve
31
Q

Functional dysphonia

A
  • Most common cause
  • Refers to voice problems with a normal larynx
  • High risk occupations where their voice is used a lot i.e. teachers
  • Called ‘muscle tension dysphonia’ its thought that altered laryngeal muscle tension causes an altered voice
  • Management- secondary care to visualise the larynx, referral to a speech therapist
  • Voice hygiene- avoid shouting/whispering and throat clearing, periods of voice rest, drink plenty of water, avoid caffeine/alcohol
32
Q

2 week wait referral

A

Used for suspected cancer, so they can see a specialist. The targets for patients with suspected cancer are to be seen within 14 days of referral, limit of 31 days from diagnosis to decision to treat and 62 days from referral to first treatment.

33
Q

Dysphonia in secondary care

A

Visualisation of the larynx is the main objective in ENT using an oendoscopy. Full examination of the neck, oral cavity, oropharynx and larynx will be undertaken.

34
Q

Types of hearing aids

A

• Behind the ear hearing aid
• In the canal hearing aid
• Bone conduction hearing aid
• Cochlear implants

35
Q

Cause of tinnitus

A

• Age related hearing loss
• Exposure to loud noise
• Stress
• Meniere’s disease – the classical symptoms of Meniere’s are hearing loss, tinnitus, aural pressure and dizziness which all come on together, in episodes lasting minutes to days
• Vestibular Schwannoma
• Medications – aspirin, diuretics, amlodipine, ototoxic medications (aminoglycoside antibiotics, chemotherapy drugs)

36
Q

Tinnitus

A

People hear high or low pitched ringing, buzzing, humming and clicking. Some people can hear their heartbeat, known as pulsatile tinnitus. This is often caused by high blood pressure, intracranial aneurysm or vascular tumours of the middle ear known as glomus tumours or most commonly because of a dysfunctional eustachian tube.

37
Q

Treatment of tinnitus

A

• Lifestyle measures= Avoid triggers – alcohol, caffeine, noise exposure. Distraction – cover up the noise with music. Stress management
• Counseling & support groups, cognitive behavioral therapy
• Hearing aids to correct hearing loss
• Noise suppression – eg. White noise generators
• Tinnitus retraining – a wearable device delivering sounds or music that masks the specific frequencies of the tinnitus and allows accustomisation to the tinnitus and distraction from the sound
• Tricyclic antidepressants (eg. Amitriptyline) if significant impact upon mood

38
Q

Conductive and sensorineural hearing loss audiograms

A

Sensorineural hearing loss audiogram- both air and bone conduction reading will be more than 20dB. May affect one or both sides.

Conductive hearing loss audiogram- Bone conduction reading will be normal i.e. between 0 to 20dB. Air conduction reading will be greater than 20dB. This is the air bone gap.

39
Q

Mixed hearing loss audiogram

A

• Air and bone readings will be more than 20dB
• However there will be a difference of more than 15dB between the two
• Bone conduction > air conduction

40
Q

Drainage of the sinus’s

A

• The frontal, maxillary and anterior ethmoids drain into the space between the inferior and middle turbinate, call the middle meatus.
• The posterior ethmoids drain into the space between the superior and middle turbinate called the superior meatus.
• The sphenoid sinus drains into the posterior part of the nasal cavity called the sphenoethmoidal recess.
• The nasolacrimal duct drains under the inferior meatus

41
Q

Difference between a polyp and a turbinate

A

Polyps are paler and have no sensory fibers. Therefore gentle touching the polyp with a probe will cause no sensation, they also tend to be mobile.

42
Q

Common causes of rhinosinusitis

A

Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis

43
Q

Rhinosinusitis- what to do if there is no improvement

A

• Nasal swab- looks for organisms resistant to penicillin
• Non contrast CT

44
Q

Complications of Rhinosinusitis

A

1) Periorbital or Orbital cellulitis. Both present with erythema and swelling around the eye, and are managed in hospital with antibiotics.
2) Subperisoteal or Orbital abscess. These occur when orbital cellulitis progresses, and requires urgent surgical intervention.
3) Meningits. This is rare but presents with severe headache, neck stiffness and photophobia
4) Subdural Abscess. Results from direct extension of infection form the sinuses and can presents with headache.
5) Cavernous sinus Thrombosis. This is very rare and presents with severe headache and orbital swelling, often bilateral.

45
Q

Rhinosinusitis- when to refer to ENT

A

1) Recurrent acute symptoms, with more than 4 attacks in a year.
2) Chronic Rhinosinusitis, with symptoms present for more than 12 weeks.
3) Subacute Rhinosinusitis, with symptoms between 4-12 weeks that are causing distress to the patient.
4) Any signs of complications of sinusitis

46
Q

Boundaries of the middle ear- roof, floor and lateral wall

A

• Roof- formed from the petrous part of the temporal bone, separates the middle ear from the middle cranial fossa. Potential route of infection in otitis media
• Floor- the jugular wall, separates the middle ear from the internal jugular vein
• Lateral wall- made of the tympanic membrane and the lateral wall of the epitympanic recess

47
Q

Boundaries of the middle ear- medial, anterior and posterior wall

A

• Medial wall- formed by the lateral wall of the internal ear. It contains a prominent bulge, produced by the facial nerve as it travels nearby.
• Anterior wall – a thin bony plate with two openings; for the auditory tube and the tensor tympani muscle. It separates the middle ear from the internal carotid artery.
• Posterior wall (mastoid wall) – it consists of a bony partition between the tympanic cavity and the mastoid air cells. Superiorly, there is a hole in this partition, allowing the two areas to communicate. This hole is known as the aditus to the mastoid antrum.

48
Q

Otitis externa

A

• Normally bacterial cause but can be fungal
Symptoms are pain, itching, discharge and hearing loss
• There is pain on palpating the tragus and moving the pinna
• Swollen, erythematous external auditory canal containing purulent discharge
• Often the tympanic membrane cant be visualised due to the swelling of the canal and discharge

49
Q

Chronic otitis media

A

Persistent or recurrent otorrhea (ear discharge) and hearing loss

50
Q

Retraction pocket with some discharge

A

• Inactive mucosal: dry perforation
• Active mucosal: wet perforation with inflamed middle ear mucosa and discharge
• Inactive squamous: retraction pocket, which has the potential to become active with retained debris (keratin)
• Active squamous: cholesteatoma

51
Q

Choleostoma

A

• A collection of benign keratinising squamous cells which are hyperproliferating
• It produces proteolytic enzymes which are locally destructive, eroding adjacent bones
• Normally managed surgically
• Dysfunction of the eustachian tube results in negative pressure in the middle ear, this sucks in the tympanic membrane forming a ‘retraction pocket’.
• Once deep enough, the pocket traps keratin debris and develops into a cholesteatoma. This can become infected leading to chronic ear discharge.
• Develop after birth
• A choleostoma can damage the facial nerve causing facial nerve palsy
• Can erode through the bone separating the middle cranial fossa, causing intracranial spread of infection i.e. intracranial abscess or meningitis

52
Q

Intracranial facial nerve anatomy

A

Arises from the pons. Travels through the internal acoustic meatus (temporal bone) via the facial canal (temporal bone), exits the cranium via the sylomastoid foramen

53
Q

Extracranial facial nerve anatomy

A

Runs through the middle ear then comes out anterior to the outer ear into the parotid gland and splits into 5 branches: Temporal, Zygomatic, Buccal, Marginal/Mandibular, Cervical.

54
Q

Upper and lower facial nerve lesions

A

• UMN- forehead spare (between motor cortex and pons)
• LMN lesion- forehead is not spared (distal to pons)

55
Q

Common causes of facial nerve palsy

A

• Intracranial (UMN) – CVA, tumour, trauma
• Intra-temporal (LMN) – complication of otitis media including cholesteatoma, temporal bone fracture
• Extracranial (LMN) – Parotid infection / neoplasia, facial trauma
• Other causes – Bell’s palsy (diagnosis of exclusion, made once other potential diagnoses ruled out), Ramsay Hunt Syndrome (varicella zoster re-activation in facial nerve), iatrogenic injury

56
Q

Complications of chronic otitis media

A

• Intratemporal- hearing loss, tympanic membrane perforation, mastoiditis, labyrinthitis, facial nerve palsy
• Intracranial- meningitis, intracranial abscess, lateral sinus thrombosis, cavernous sinus thrombosis, subdural empyema

57
Q

Perforation of the tympanic membrane

A

• Can occur with otitis media
• If the ear is actively discharging, antibiotics and steroid drops can be prescribed
• The perforation should be kept dry i.e. free from infection and may heal by itself
• Surgical repair of the tympanic membrane can be performed using cartilage or fascia (myringoplasty) which prevents future infections
• Most tympanic membrane perforations heal within 3 months

Medicine year 3- EOCP (27 decks)

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