Localizing signs: You can localize brainstem strokes by recognizing the deficits caused by involvement of specific cranial nerves:
III or IV cranial nerve: Midbrain lesion
V cranial nerve: Rostral pontine lesion
VI, VII, and VIII nerves: Caudal pontine lesion
IX, X, and XII nerves: Medullary lesion (bulbar signs)
Parinaud’s syndrome: Also called dorsal midbrain syndrome or pretectal syndrome. It results from lesions in the dorsal midbrain region, most commonly due to pineal gland tumors, brainstem hemorrhage, and infarcts.
It presents with paralysis of vertical gaze, often with downward deviation of both eyes (the “setting sun” sign). Other findings include dilated and fixed pupils, lid retraction, and nystagmus.
The light reflex is lost, while the accommodation reflex may or may not be lost. Light-near dissociation refers to poor bilateral pupillary constriction in response to light, with preserved constriction during convergence.
Vertical gaze palsy occurs due to damage to the vertical gaze center (the rostral interstitial nucleus of the medial longitudinal fasciculus and the interstitial nucleus of Cajal) and its connections.
Collier sign (bilateral lid retraction) occurs because inhibitory supranuclear input to the III nerve nucleus is lost, leading to constant stimulation of the levator palpebrae superioris.
Pontocerebellar angle syndrome: Seen with tumors or masses in the cerebellopontine angle, such as schwannomas (acoustic neuromas), meningiomas, aneurysms, etc.
It presents with tinnitus, loss of balance, sensorineural hearing loss, dizziness, vertigo, and ataxia. In late stages, it may present with ipsilateral facial weakness and paresis of the muscles of mastication.
TIA: A transient ischemic attack is a transient stroke that lasts only a few minutes. It is caused by microembolization from an atherosclerotic plaque.
Most symptoms of a TIA disappear within an hour, although they may persist for up to 24 hours.
Symptoms include numbness or weakness in the face, arm, or leg (especially on one side of the body); confusion or difficulty talking or understanding speech; trouble seeing in one or both eyes; difficulty walking; dizziness; or loss of balance and coordination.
Thalamic pain syndrome or Déjérine-Roussy syndrome: A lesion localized to the ventral posterolateral nucleus in the thalamus leads to an initial loss of all sensations from the contralateral side of the body, including pain.
Over time, the patient may experience pain in all or part of the contralateral side of the body. This is referred to as thalamic pain syndrome.
About one-third of those who have a TIA will have an acute stroke sometime in the future. The most important treatable factors linked to TIAs and stroke are high blood pressure, cigarette smoking, heart disease, carotid artery disease, diabetes, and heavy use of alcohol.
Carotid artery stenosis: Caused by atherosclerosis of the carotid arteries or, rarely, by fibromuscular dysplasia. It carries a high risk of causing stroke.
It is asymptomatic in most cases. Symptomatic carotid artery stenosis presents with “amaurosis fugax”, contralateral weakness or numbness of an arm, leg, or the face, dizziness, dysarthria, and aphasia.
Amaurosis fugax is due to cholesterol embolization from atherosclerotic plaques in the carotid artery to the retinal artery. It presents with sudden, painless loss of vision (like a curtain coming down), followed by restoration of vision (curtain raising up).
Carotid bruits can be auscultated in carotid stenosis.
Invasive treatment is considered for symptomatic patients with stenosis greater than 50% and asymptomatic patients with stenosis greater than 60%. Carotid endarterectomy (preferably within two weeks of symptoms) or carotid angioplasty with stenting are the preferred procedures. Asymptomatic patients are managed with medical therapy and lifestyle modifications.
Arteriovenous malformations of the brain: A developmental anomaly of blood vessels consisting of tangled, poorly formed vessels between a feeding artery and a draining vein, without a capillary network in between.
It can cause SAH or intracerebral hemorrhage. It may cause seizures and neurological deficits and can be associated with aneurysms. They are most common in MCA territory.
It has a characteristic “bag of worms” appearance on CT with contrast.
Posterior reversible encephalopathy syndrome: Presents with rapid onset of headache, seizures, altered sensorium, and visual deficits, with reversible changes that resolve over days to weeks.
It is associated with renal disorders (chronic kidney disease and acute kidney injury), hypertension, organ transplantation, immunosuppressive drugs, SLE, and TTP.
It is postulated to result from loss of autoregulation of blood flow to the brain or from systemic inflammation.
Inherited risk factors
Acquired risk factors
| Parameter | Normal finding |
| Appearance | Clear, colorless |
| Pressure | 100-180 mm of H2O (8-15 mm Hg) |
| Protein | 15-45 mg/dl |
| Glucose | 50-80 mg/dl (⅔ rd of blood glucose) |
| Cells | 0-5 mononuclear cells; no neutrophils or polymorphs; few RBCs if traumatic tap |
| Abnormal finding | Common causes |
| Neutrophils or polymorphs | Bacterial infections like meningitis |
| Increased lymphocytes | Viral infections, tuberculous meningitis, multiple sclerosis, malignancies, fungal meningitis |
| Increased protein* | Bacterial meningitis, tumors, SAH, cerebral infarcts,GBS, MS (IgG, Myelin basic protein) |
| Low glucose** | Bacterial meningitis, fungal infections, tuberculosis, sarcoidosis, tumors, mumps, HSV and lymphocytic choriomeningitis virus infections |
| Blood/RBCs | Traumatic tap (clears out towards the end), SAH (uniformly red, does not clear out), |
| Pink color | Oxyhemoglobin from RBC lysis, first seen at 2-4 hours and disappears by 1 week. |
| Yellow color or xanthochromia | Bilirubin, first seen at 12 hours after SAH and disappears by 2-4 weeks |
| Albumin and prealbumin | Inflammation, increased vascular permeability |
| Gamma globulin | MS, SSPE, general paresis, herpes encephalitis, myxedema, carcinomatous cerebellar degeneration, connective tissue disease. |
| Myelin basic protein or MBP*** | Increased in MS, spinal cord demyelination, HTLV associated myelopathy. Decreases in remission of MS. |
| tau proteins | Both t-tau and p-tau are increased in Alzheimer’s disease, while only t-tau is elevated in CJD. |
| 14-3-3 proteins | CJD, stroke, encephalitis |
| S100B | CNS trauma, stroke, HIE, brain melanoma, Alzheimer’s disease, Frontotemporal dementia, MS. |
* The CSF index is the CSF IgG to CSF albumin ratio compared to the serum IgG to serum albumin ratio. Any increase in the index reflects IgG production in the CNS. Raised CSF IgG index is seen in multiple sclerosis, neurosyphilis, SSPE, polyradiculopathy, etc.
** CSF glucose is normal in viral meningitis, neurosyphilis, and demyelinating diseases
*** Oligoclonal bands will be seen in CSF in multiple sclerosis (MS).
Dandy Walker Syndrome: Characterized by underdevelopment of the cerebellar vermis, cystic enlargement of the IVth ventricle, and enlargement of the posterior cranial fossa.
Causation is multifactorial, with a few cases showing deletion of chromosome 3q, 6p, 13q, or duplication of 9p. It affects more females than males.
It presents with developmental delay, hypotonia or spasticity, mental retardation, seizures, poor coordination and balance (ataxia), and sometimes enlarged head circumference and increased pressure within the skull due to hydrocephalus. Severe cases may show respiratory failure.
Imaging studies show classic mega-cisterna magna (enlargement of the cisterna magna).
Facial nerve (VII cranial nerve) palsy: Most cases are idiopathic. Known causes include Lyme disease, HSV, HZV, Coxsackie virus, Adenovirus, CMV, EBV, Measles, Mumps, Rubella and Influenza B viruses, head trauma, sarcoidosis, iatrogenic injury during surgery of the parotid gland, forceps delivery, etc.
Swelling of the facial nerve from viral or immunological disorders can cause palsy.
The motor nucleus of the VII nerve supplies the muscles of facial expression, stapedius, stylohyoid, and the posterior belly of the digastric muscle.
Corticobulbar fibres arise from the motor cortex. They provide:
The facial nerve exits at the stylomastoid foramen and becomes extracranial.
Patients with facial nerve palsy typically present with pain behind the ear, followed a few hours later by facial weakness and paralysis.
Hyperacusis (hypersensitivity to loud sounds) occurs due to paralysis of the stapedius. Patients may be unable to show their teeth, and the nasolabial folds flatten out.
Ramsay Hunt syndrome is caused by reactivation of VZV and presents with facial paralysis, herpetiform vesicular eruptions, and vestibulocochlear dysfunction.
Depending on the location of the lesion, facial nerve palsy can be UMN or LMN. Idiopathic LMN facial palsy is also called Bell’s palsy.
Differentiating features between upper and lower motor neuron facial palsy