Neuro Flashcards
Anterior Spinal Artery infarct
Anterior spinal artery infarctions can occur after damage to the aorta, including both aneurysm repair and dissection.
single anterior spinal artery running down the midline of the spinal cord (in the anterior median fissure), blockage causes loss of pain, temperature, motor and autonomic function below that level.
Dorsal column function is preserved.
Causes of autonomic neuropathy
Diabetes mellitus
Infections (including HIV, lyme and chagas)
Autoimmune disease (including SLE)
Amyloidosis
Bell’s Palsy
Acute (but not sudden) onset, unilateral, lower motor neuron facial weakness, sparing the extraocular muscles and muscles of mastication.
Mild-moderate postauricular otalgia (which may precede paralysis).
Hyperacusis (actually quite uncommon).
Nervus intermedius symptoms (altered taste and dry eyes/mouth).
Bell’s Palsy management
he central component of Bell’s Palsy management is the prompt administration of oral steroids: 50mg OM for 10 days, followed by a taper.
Supportive treatments including artificial tears and ocular lubricants, and an eye patch/tape (especially if protective Bell’s phenomenon is absent) should be considered
Erb’s palsy
Involves the C5-6 nerve roots with corresponding dermatomal sensory loss, and the so-called “waiter’s tip” sign with shoulder adduction, elbow extension, forearm pronation and wrist flexion. It is most typically associated with shoulder dystocia and traumatic childbirth.
Klumpke’s palsy
Involves the C8-T1 nerve roots with corresponding dermatomal sensory loss, and weakness of the intrinsic muscles of the hand. Uncommonly, T1 involvement may also result in an ipsilateral Horner’s syndrome
Brown-Sequard Syndrome
Disruption of descending lateral corticospinal tracts, ascending dorsal column and ascending spinothalamic tracts leads to the following findings below the level of the injury:
Ipsilateral hemiplegia
Ipsilateral loss of proprioception and vibration
Contralateral loss of pain and temperature sensation
Common causes of BSS include:
Brown-Sequard Syndrome
Cord trauma (penetrating injuries being the most common) Neoplasms Disk herniation Demyelination Infective/ inflammatory lesions Epidural hematomas
Bulbar palsy
bulbar palsy is a ‘lower motor neurone’ lesion affecting cranial nerves 9, 10 and 12
Clinical signs include an absent or normal jaw jerk reflex, an absent gag reflex, a flaccid fasciculating tongue, nasal quiet speech, and signs suggestive of the cause e.g. limb fasciculations of motor neurone disease.
Cauda Equina Syndrome
management
Management
Patient with clinical features suggestive of spinal cord compression or cauda equina syndrome should have an urgent WHOLE spine MRI, with an aim (in appropriate cases) to surgically decompress within 48 hours.
In patients where malignancy is demonstrated on MRI, or in patients where clinical suspicion is high, administration of dexamethasone 16 mg daily in divided doses (with PPI cover) is indicated.
he features of cerebellar dysfunction can be remembered by the acronym DANISH:
Dysdiadochokinesia (an inability to perform rapid alternating hand movements)
Ataxia (a broad-based, unsteady gait)
Nystagmus (involuntary eye movements)
Intention tremor (seen when the patient is asked to perform the ‘finger-nose test’)
Slurred speech
Hypotonia
Cervical Spondylosis
Manifestations include:
Neck pain
Radiculopathy due to compression of nerve roots at the site of foraminal exit
Myelopathy, probably due to dynamic stretch of the spinal cord over impinging spinal osteophytes.
On examination, neck pain is accompanied by flaccid upper limb paresis (due to radiculopathy), variable sensory changes (sometimes including the Lhermitte phenomenon), and spastic paraparesis (with variable involvement of the upper limbs depending on the site of the lesion, and degree of radiculopathy).
Charcot-Marie-Tooth Syndrome
most common being an autosomal dominant mutation in the peripheral myelin protein 22 gene (PMP22..
There are two broad groups of disease: type 1 which is a demyelinating condition which is more common (and includes the PMP22 subtype), and type 2 which is axonal.
Clinical features
As disease progresses (most commonly over decades) some key clinical features may be noted: (1. thickening and enlargement of the nerves themselves, (2. symmetrical distal muscular atrophy (champagne bottle legs, and claw hand), and (3. pes cavus (high-arched feet).
Diagnosis
Diagnosis is made with a combination of nerve conduction studies and genetic testing. Patients with type 1 have reduced conduction velocity, whereas this is normal in type 2. While the disease may be incurable, most have a normal lifespan with expert supportive management. Majority require walking aids eventually, though requiring a wheelchair is uncommon.
Clinical features of Huntington’s disease
It is characterised by the triad of
Dominant inheritance
Choreoathetosis
Dementia
MRI and CT scans in moderate to severe disease can show loss of striatal volume and increased size of the frontal horns of the lateral ventricles.
Management of Huntington’s disease
Patients and their families require a significant amount of physical and emotional support from a multidisciplinary team.
Chorea can be managed with a number of medications, with tetrabenazine having the most evidence-base.
Depression can be treated with Selective serotonin reuptake inhibitors (SSRIs) as a first choice.
Psychosis can be managed with antipsychotics, preferably newer atypical agents due to lower rates of extrapyramidal side effects.
most common cause of Encephalitis
herpes simplex virus type 1
Investigating encephalitis
Encephalitis should be suspected in any patient with sudden onset behavioural change, new seizures and unexplained acute headache with meningism.
Standard work up for encephalitis is similar to that for meningitis, with a routine panel of blood tests, blood cultures and viral PCR. CSF should also be sent for viral PCR in addition to standard tests, and malaria blood films should be considered if exposure is suspected.
CNS imaging may also be helpful – HSV has a predilection for the temporal lobes and bilateral multifocal haemorrhage is typical.
treatment of encephalitis
Treatment of suspected encephalitis is empirical and should involve broad spectrum antimicrobial cover with 2g IV ceftriaxone BD and 10 mg/kg aciclovir TDS for two weeks.
Supportive management of complications including prompt termination of seizure activity with anticonvulsants (such as phenytoin) also important.
clinical presentation - Absence seizures
Patients, often children, pause briefly, for less than 10 seconds, and then carry on where they left off.
Treatment: Ethosuximide 1st line Sodium Valproate (SE: weight gain, hair loss which grows back curly, oedema, ataxia, tremor, teratogenicity)
Tonic-clonic seizures:
Patients lose consciousness; their limbs stiffen (tonic) and start jerking (clonic). Post-ictal confusion is common.
Treatment: Sodium Valproate or Lamotrigine is first-line.
Myoclonic seizures:
udden jerk of a limb, trunk, or face.
Treatment: Sodium Valproate is first-line unless the patient is a female of childbearing age where Levetiracetam or Topiramate should be used instead as first-line; avoid Carbamazepine as it worsens seizures.
Atonic seizures:
Atonic seizures: Sudden loss of muscle tone, causing the patient to fall, whilst retaining consciousness. Treatment: Sodium Valproate or Lamotrigine is first-line.
Essential tremor
mainly the upper limbs distally and is postural or kinetic.
amplitude increases with time, and patients experience difficulty in writing, eating, holding objects and doing fine motor tasks, dressing, and speaking
increares with stress
Essential tremor management
Management
The management of a patient with ET includes:
Behavioural techniques and physical therapy Medical (pharmacological) therapy (with agents such as propranolol, primidone, topiramate, gabapentin, clonazepam etc.) Surgical treatment (such as deep brain stimulation, focused ultrasound thalamotomy and radiosurgical (Gamma Knife) thalamotomy)
Extradural Haemorrhage
brief loss of consciousness, followed by regaining of normal consciousness level (the lucid interval), with subsequent deterioration of consciousness and headache.
Other causes of peripheral nerve disease include:
Other causes of peripheral nerve disease include:
Physical lesions of the cerebellopontine angle (including the classical acoustic neuroma)
Basal meningitis (which is often bilateral and may be infective or inflammatory, including lyme disease and sarcoidosis).
Ramsay Hunt syndrome (herpes zoster of the facial nerve)
Trauma
Diseases of the middle/inner ear
Mononeuritis multiplex
Fibromuscular dysplasia
Fibromuscular dysplasia (FMD), formerly called fibromuscular fibroplasia, is a group of non-atherosclerotic, non-inflammatory arterial diseases that most commonly involve the renal and carotid arteries.
Causes of Foot Drop
L5 root lesion (radiculopathy) – distinguished by loss of inversion (inversion is a tibial nerve function and is not lost in patients with a common peroneal nerve lesion). Sensory loss is over the L5 dermatome, and sciatica-type shooting leg pain may also be present. Lumbosacral disc herniation is the most common cause.
Distal motor neuropathy – often associated with glove and stocking sensory disturbance, and loss of all movements of the foot.
Small cortical lesions – often with though other upper neuron features may be present.
Uncommonly: intrinsic cord disease, partial sciatic nerve disease and myopathy may also mimic foot drop.
Friedreich’s ataxia
autosomal recessive trinucleotide repeat disorder resulting in reduced level or function of the frataxin protein.
Patients typically present in their teenage years with lower limb weakness, gait abnormalities, or falls.
On physical examination there may be cerebellar signs (due to involvement of the spinocerebellar tracts) or mixed upper and lower motor neurone signs e.g. absent knee/ankle reflexes but upgoing plantars (due to involvement of the corticospinal tracts and peripheral nerves).
Involvement of the dorsal columns can lead to impaired joint/vibration sense. Other clues on physical examination include a high-arched palate, pes cavus, and kyphoscoliosis.
Non-motor features include: hypertrophic obstructive cardiomyopathy, reduced visual acuity, type 1 diabetes mellitus, and deafness.
Miller-Fisher syndrome
(a variant of GBS) presents with ataxia, ophthalmoplegia, and areflexia. The condition is typically positive for anti-GQ1b antibodies.
Acute management of haemorrhagic stroke
Neurosurgical and neurocritical care evaluation due to the potential for surgical intervention (e.g. decompressive hemicraniectomy).
Admission to the neuro ICU or stroke unit (the patient may require intubation and ventilation or invasive monitoring of ICPs).
Aim to keep blood pressure <140/80 as poor blood pressure control in the acute stage is associated with poorer outcomes later on
Diagnosis of Migraine
Presence of an aura confirms the diagnosis. Otherwise, in headaches with no aura, the following criteria is required - at least 5 headaches lasting 4-72 hours, with nausea/vomiting or photo/phonophobia AND 2 of: unilateral headache, pulsating character, impaired or worsened by daily activities.
Management of Migraine
Avoid triggers; prophylaxis with Propranolol (CI: asthma) or Topiramate;
managing an acute attack with an oral triptan such as Sumatriptan (CI: ischaemic heart disease), in addition to Paracetamol or an NSAID. Ensure that female patients are not taking combined oral contraceptive pills as it increases their risk of ischaemic stroke.
