Aneurysm of the posterior communicating artery (painful)
Mononeuritis in DM (pupil usually normal)
Pathology beside the cavernous sinus, in the superior orbital fissure or in the orbit (adjacent nerves commonly involved, e.g. IV, VI, Va, and II if in the orbit)
"Coning" of the temporal lobe
Notes about innervation of the eyelids and pupil
The eyelid is kept up by levator palpebrae superioris, which has two sources of innervation, minor from the sympathetic nervous system, major from III
Pupillary dilatation is activated by the sympathetic nervous system, and is adrenergic
Pupillary constriction is mediated throught the parasympathetic component of III and is cholinergic
Bell's Palsy
Symptoms and signs
Unilateral paralysis of the muscles of facial expression (without forehead sparing)
Pain behind the ear at onset is common
Hyperaccusis and loss of taste (if the lesion is within the petrous temporal bone)
Differential diagnoses (Bell's is a diagnosis of exclusion)
Trauma
Middle ear infection
Ramsey Hunt syndrome (must examine ear canal for vesicles)
Tumours (e.g. glomus tumour)
Horner's Syndrome
Signs:
Ptosis
Meiosis (constricted pupil)
Anhydrosis - on the same side of the face or body, the extent depending on the level of the lesion
Enophthalmos
Causes - Lesion in the ipsilateral sympathetic pathway
Carcinoma of bronchus - Pancoast's tumour
Syringomyelia (UMN signs in legs, LMN signs in arms)
V, VI, VII & VIII arise in the pons, though VI doesn't appear to be affected
V, VII & VIII combined malfunction together with ipsilateral cerebellar incoordination suggests a lesion in the cerebellopontine angle
Effects of an VIII lesion
Sensorineural deafness
VI, VII & V lesions occur (corneal reflex is first to go), followed by:
Cerebellar signs (ipsilateral)
Later, Pyramidal signs (contralateral)
Nystagmus is often present
Causes (of that VIII lesion) include:
Acoustic neuroma (common OSCE)
Meningioma and secondary neoplasm
Carcinomatous meningitis
Inflammatory lesions
Acoustic neuroma is a benign tumour of the Schwann cells of VIII. Providing it is diagnosed early it can be removed. If not it will enlarge to demonstrate the features of a cerebellopontine angle tumour (see above, with symptoms of increased ICP)
Bulbar (Medulla) Palsy
Due to bilateral (LMN) impairment of function in IX, X & XII
Features of syndrome:
Dysarthria
Dysphagia, often with choking episodes and/or nasal regurgitation of fluids
Dysphonia and poor cough, because of weak vocal cords
Susceptibility to aspiration pneumonia
Autonomic abnormalities are uncommon
Common causes
MND
Guillain-Barre
Myasthenia gravis
Pseudo-bulbar Palsy
Bilateral supranuclear (UMN) lesions of the lower cranial nuclei producing weakness and poverty of movement of the tongue and pharyngeal muscles.
Clinical findings:
Stiff, slow, spastic tongue (which is not wasted)
Dysarthria with a stiff, slow, spastic voice, which sounds dry and gravelly
Dysphagia
Gag reflex and palatal reflex are preserved
Jaw jerk is exaggerated
Emotional lability (inappropriate laughing or crying) often accompanies
Principle causes:
MND, in which there are often both UMN & LMN lesions (i.e. elements of both pseudobulbar and bulbar palsy)
MS, in which it occurs mainly as a late event
Cerebrovascular disease, in which it may occur with multi-infarct dementia
Following severe head injury
Great difficulty with swallowing, dysarthria and a slow moving tongue also develop in the late stages of Parkinson's. This is aetiologically distinct from both bulbar and pseudo-bulbar palsy.
Gaze Palsies
Supranuclear gaze palsy
Caused by a major acute hemispherical lesion (massive stroke, severe head injury)
Patient is unable to initiate movement (and therefore gaze) to the contralateral side
Reflex conjugate eye movement is preserved
Classic picture = Eyes deviated to the right (due to a right hemisphere lesion) but able to reflexly induce conjugate eye movements e.g. by caloric stimulation of the ears or by rapid doll's head movements of the head from side to side
Internuclear ophthalmoplegia - not really a gaze palsy
A lesion between the 3rd nerve nucleus in the midbrain and the 6th nerve nucleus in the pons (on the right, for example)
Does not affect activation of the left VI
Does interfere with activation of the right III, so that ADduction of the right eye may be slow, incomplete or paralysed
Basically looks like paralysis of the ipsilateral medial rectus muscle
Convergence is normal
Cause if young = MS
Cause if old = cerebrovascular disease
Brain-stem Infarction
Would, presumably, give you the symptoms in the CNs that have their nuclei in the part of the brainstem infarcted, if they are still alive:
Pons = III & IV
Midbrain = V - VIII
Medulla = IX, X & XII
Multiple Sclerosis
Internuclear ophthalmoplegia is almost pathogneumonic for MS
Motor Neurone Disease
Frequently causes bulbar palsy. Inanition and aspiration pneumonia are frequently causes of death. The tongue is small, weak or immobile, and fasciculating
Myasthenia Gravis
Muscle weakness, with abnormal fatiguability and improvement after rest, characterises myasthenia
Symptoms tend to be worse at the end of the day, and after repetitive use of muscles for a particular task, e.g. chewing and swallowing may be much more difficult towards the end of a meal than they were at the start.
Ocular involvement is common
Myasthenia should be considered in any unexplained ophthalmoplegia, even if it looks like a 4th, 6th or partial 3rd nerve palsy
Frequency of muscle involvement:
External ocular => Double vision and ptosis (common)
Bulbar => Difficulty chewing, swallowing and talking
Neck => Difficulty lifting head up from lying position
Proximal limb => Proximal weakness
Trunk => Breathing problems and difficulty in sitting up from lying down
Distal limb => Weak hand-grips, ankles and feet (rare)
