hidrocefalia

Palpable open fontanelles in a young dog are most consistent with: Congenital hydrocephalus. Normal adult anatomy. Peripheral neuropathy. Lumbar spinal cord disease.

Blindness with normal ocular examination in hydrocephalus indicates: Spinal cord compression. Primary retinal disease. Central (forebrain) dysfunction. Peripheral nerve lesion.

Pacing and circling behavior in hydrocephalus reflect: Lumbar spinal cord lesion. Peripheral vestibular disease. Forebrain disease. Myopathy.

A young toy breed puppy with a dome-shaped skull and delayed learning most likely has dysfunction of the: Peripheral nerve. Lumbar spinal cord. Neuromuscular junction. Forebrain.

Clinical progression in congenital hydrocephalus is described in the notes as: Variable, with possible delayed onset. Always static and non-progressive. Always rapidly progressive. Always fatal in neonatal period.

The primary anatomical change in active hydrocephalus is: Peripheral nerve demyelination. Ventricular distension. Spinal cord compression only. Primary cerebellar atrophy.

The goal of ventriculoperitoneal shunting is to: Increase CSF pressure. Stimulate brain tissue regeneration. Establish controlled diversion of CSF. Correct skull conformation.

Congenital hydrocephalus most often becomes clinically evident: Exclusively in geriatric dogs. Only after 8 years of age. Only after spinal trauma. During the first months of life.

A dome-shaped skull in congenital hydrocephalus is primarily associated with. Acquired traumatic brain injury. Normal aging changes. Congenital hydrocephalus in toy breeds. Peripheral neuropathy.

The main therapeutic aim in managing hydrocephalus is to: Remove all brain tissue damage. Eliminate skull deformities. Control CSF accumulation and ventricular distension. Increase CSF production.

The primary objective of medical therapy in hydrocephalus is to: Eliminate congenital malformations. Decrease CSF production. Stimulate CSF overproduction. Increase skull size.

Clinical signs of congenital hydrocephalus may go unrecognized initially because: Onset may be delayed and progression variable. Imaging cannot detect ventricular enlargement. Only geriatric dogs are affected. Hydrocephalus never causes signs.

Which statement correctly matches the notes regarding internal and external hydrocephalus?. Internal: always acquired; External: always congenital. Internal: CSF accumulation within the subarachnoid space External: CSF accumulation within the ventricular system. Internal: defined by seizures; External: defined by blindness. Internal: CSF accumulation within the ventricular system External: CSF accumulation within the subarachnoid space.

A realistic goal of medical therapy in hydrocephalus is to: Reduce CSF production and provide symptomatic relief. Cure congenital malformation. Close cranial sutures permanently. Stimulate new brain growth.

In the therapeutic protocol described in the lecture notes, acute cases managed in hospital include use of: Chemotherapy as first-line therapy. No intervention until the dog is adult. Ventriculoperitoneal shunting as the first step in all cases. Mannitol.

Delayed onset of signs in congenital hydrocephalus suggests: Variable progression of ventricular distension. Absence of congenital abnormality. Peripheral nerve adaptation. Complete spontaneous resolution.

The clinical course of congenital hydrocephalus is described as: Always static and non-progressive. Always rapidly progressive and fatal. Always improving spontaneously. Variable with possible delayed onset.

In communicating hydrocephalus, CSF within the ventricles: Is replaced by blood. Is absent. Communicates with the subarachnoid space. Is completely isolated.

Overall management of hydrocephalus requires: Immediate surgery in all cases. Assessment of severity, progression and response to therapy. Treatment only if seizures occur. No follow-up once diagnosed.

Why must clinical signs be evaluated alongside imaging findings?. Skull shape determines diagnosis. Seizures automatically confirm hydrocephalus. MRI cannot detect ventricles. Ventricular enlargement alone does not confirm clinical hydrocephalus.

The primary target of medical therapy for hydrocephalus described in the review is to: Close cranial sutures. Decrease CSF production. Repair cerebellar vermis hypoplasia. Increase absorption at arachnoid villi.

Obstruction of CSF flow typically leads to: Decreased CSF volume. Ventricular dilation proximal to the obstruction. Peripheral nerve dysfunction. Immediate skull shrinkage.

A young Chihuahua with open fontanelles and behavioral abnormalities should be evaluated for: Congenital hydrocephalus. Intervertebral disc disease. Myasthenia gravis. Peripheral neuropathy.

Which statement best matches the treatment approach described in the lecture notes and review for canine hydrocephalus?. Treatment decisions are based only on ventricular size on imaging. Medical therapy aims to increase CSF production; surgery aims to stop CSF circulation completely. Medical therapy aims to decrease CSF production; surgical shunting aims to establish controlled CSF flow. Medical therapy is always curative; surgery is only for mild cases.

According to the notes, hydrocephalus is best defined as: A condition defined by CSF accumulation only in the spinal subarachnoid space. An active distension of the ventricular system due to inadequate movement of CSF from production (within ventricles) to absorption. A disorder caused only by increased CSF production. Any ventricular asymmetry seen on imaging, regardless of clinical signs.

The prognosis of hydrocephalus depends primarily on: Sex of the patient. Coat color. Owner compliance alone. Severity of neurological deficits and response to treatment.

Open cranial sutures in puppies with hydrocephalus allow: Immediate resolution of CSF imbalance. Reduced ventricular size. Peripheral nerve compression. Expansion of the skull with dome-shaped appearance.

The dome-shaped skull seen in congenital hydrocephalus is related to: Normal toy breed conformation unrelated to CSF. Primary cerebellar hypoplasia. Expansion of skull bones due to increased intracranial pressure in young animals. Muscle hypertrophy of the temporalis.

Medical treatment of hydrocephalus is generally considered: Often palliative and aimed at controlling clinical signs. Focused on peripheral nerve repair. Always curative. Unnecessary in mild cases.

Medical therapy does not permanently correct hydrocephalus because it: Does not resolve the underlying CSF flow disturbance. Repairs lost brain tissue. Closes cranial sutures. Increases CSF production.

The 'sun-setting' eye appearance in hydrocephalus refers to: Bilateral ventrolateral strabismus. Miotic pupils with nystagmus. Exophthalmos. Dorsal strabismus with head tilt.

Congenital hydrocephalus most commonly affects: Young toy breed dogs. Geriatric large breed dogs. Working dogs over 8 years. Adult mixed breed dogs exclusively.

Obstruction within the ventricular system before CSF reaches the subarachnoid space results in: Noncommunicating (obstructive) hydrocephalus. Peripheral nerve damage. Hydrocephalus ex-vacuo. Normal ventricular anatomy.

In acquired hydrocephalus, ventricular enlargement commonly occurs secondary to: Peripheral neuropathy. Age-related atrophy only. Normal toy breed skull shape. Mass or swelling obstructing CSF flow.

In a dog with rapidly worsening neurological signs despite medical therapy, the most appropriate next step is to: Stop all treatment. Consider ventriculoperitoneal shunting. Ignore imaging findings. Treat as peripheral neuropathy.

External hydrocephalus involves dilation of the: Subarachnoid space. Cranial sutures. Spinal cord grey matter. Peripheral nerve sheath.

Which breed is listed in the notes as overrepresented (higher risk) for congenital hydrocephalus?. Labrador Retriever. Greyhound. German Shepherd Dog. Chihuahua.

A dome-shaped skull in a young dog should prompt evaluation for: Congenital hydrocephalus. Cervical spondylomyelopathy. Peripheral nerve disease. Myopathy.

Which combination of clinical features is described in the review as possible with post-shunting infection in dogs?. Isolated pelvic limb lameness with joint swelling. Polyuria and polydipsia only. Pruritus and otitis externa. Circling, generalised trembling, proprioceptive deficits, vertical nystagmus, head tilt, and cervical spinal pain.

In the notes, hydrocephalus is divided into which two main etiologic categories?. Congenital hydrocephalus and acquired hydrocephalus. Internal hydrocephalus and external hydrocephalus. Acute hydrocephalus and chronic hydrocephalus. Communicating hydrocephalus and noncommunicating hydrocephalus.

Surgical treatment should be considered when: Only seizures are present without other signs. Neurological deficits are severe, progressive, or unresponsive to medical therapy. The dog is a toy breed. Ventricular enlargement is minimal and asymptomatic.

Open cranial sutures in young animals may result in: Expansion of the skull with dome-shaped appearance. Peripheral nerve stretching. Reduced CSF production. Immediate brainstem compression.

Which set includes drugs specifically listed in the review as commonly used to decrease CSF production in hydrocephalus?. Phenobarbital, potassium bromide, and diazepam. Acetazolamide, furosemide, and prednisone. Meloxicam, amoxicillin, and maropitant. Omeprazole, insulin, and atropine.

Behavioral abnormalities in hydrocephalus are attributed to: Peripheral nerve injury. Cervical disc disease. Forebrain dysfunction. Neuromuscular disease.

Which sign most strongly indicates forebrain dysfunction in hydrocephalus?. Flaccid paralysis of limbs. Behavioral abnormalities and altered mentation. Reduced peripheral reflexes only. Muscle fasciculations.

Ongoing assessment in hydrocephalus patients is important to evaluate: Coat color changes. Peripheral reflexes exclusively. Skull shape only. Clinical severity and progression.

The ventriculoperitoneal shunt diverts CSF to the: Subarachnoid space. Spinal canal. Thoracic cavity. Peritoneal cavity.

After initiating treatment for hydrocephalus, regular monitoring is necessary to assess: Peripheral nerve conduction speed. Neurological progression and response to therapy. Coat color changes. Body weight only.

Medical therapy for hydrocephalus is generally considered: Focused on increasing CSF pressure. Always curative. Unnecessary in congenital cases. Often palliative and aimed at reducing CSF production.

The rationale for ventriculoperitoneal shunting is to: Increase CSF production. Close cranial sutures. Remove skull deformities. Divert CSF to control ventricular enlargement.

The goal of ventriculoperitoneal shunting is to: Increase CSF production. Establish controlled CSF flow and reduce ventricular distension. Close cranial sutures. Eliminate all seizure activity permanently.

According to the documents, surgical management is recommended when hydrocephalus results in: Severe or progressive neurological deficits, or failure of medical management. Only when the fontanelle is palpable. Only when seizures are absent. Any ventriculomegaly on imaging even if the dog is normal.

Acquired hydrocephalus may develop secondary to: Open fontanelles in neonates. Physiological brain aging. Obstruction of CSF flow by a mass or swelling. Normal ventricular asymmetry.

Circling behavior in hydrocephalus reflects dysfunction of the: Peripheral nerves. Peripheral vestibular system only. Thoracolumbar spinal cord. Forebrain.

Decreased vision or blindness in hydrocephalus is most consistent with dysfunction of the: Peripheral nerve only. Lumbar spinal cord. Neuromuscular junction. Forebrain.

Ventriculoperitoneal shunting works by: Diverting CSF to establish controlled flow. Removing skull bone. Closing open fontanelles. Increasing CSF production.

In the notes, obstructive (noncommunicating) hydrocephalus is described as: Ventricular dilation caused by obstruction of CSF flow before it enters the subarachnoid space. CSF accumulation within the subarachnoid space only. A normal age-related increase in CSF volume in older animals. A condition where CSF production stops completely.

Which combination of signs best supports a forebrain localization in hydrocephalus?. Muscle atrophy and fasciculations. Head tilt and positional nystagmus. Behavioral change, seizures, and central blindness. Flaccid paresis with decreased reflexes.

When enlarged ventricles are identified on imaging, clinicians must: Diagnose hydrocephalus immediately. Assume severe neurological dysfunction. Interpret findings in conjunction with clinical signs. Ignore the imaging result.

Medical therapy in hydrocephalus is often described as: Curative in all cases. Unnecessary in congenital cases. Focused on increasing CSF pressure. Palliative and aimed at reducing CSF production.

According to the notes, clinical signs of congenital hydrocephalus most commonly become apparent: Only after cranial sutures have closed in adulthood. Only after 6 years of age. Only in geriatric animals due to normal aging. In the first few months of life (although signs may be present from birth).

Neurological dysfunction in dogs with hydrocephalus most commonly localizes to the: Forebrain. Peripheral nerve. Cervical spinal cord. Neuromuscular junction.

Bilateral ventrolateral strabismus (“sun-setting” eyes) in hydrocephalus is associated with: Vestibular disease. Spinal cord compression. Peripheral nerve paralysis only. Congenital hydrocephalus.

Seizures in hydrocephalus patients indicate involvement of the: Neuromuscular junction. Forebrain. Peripheral nerve. Spinal cord only.

Medical therapy in hydrocephalus is generally considered limited because it: Always cures the condition. Eliminates congenital abnormalities. May be palliative and not permanently correct CSF flow disturbance. Increases CSF production.

Congenital hydrocephalus progression is described as: Always acute and rapidly fatal. Always static without change. Variable with possible delayed onset. Always resolving spontaneously.

Acquired hydrocephalus is most commonly associated with: Open cranial sutures. Obstruction of CSF flow by masses or swelling. Toy breed genetics only. Peripheral nerve injury.

According to the notes, communicating hydrocephalus typically results from: Primary loss of CNS parenchyma with CSF occupying the void. A lesion obstructing CSF flow before it enters the subarachnoid space. An obstruction beyond the fourth ventricle with persistence of communication between ventricular system and subarachnoid space. Skull malformation causing domed head without CSF flow disturbance.

Clinically significant hydrocephalus requires: Imaging alone. Skull shape only. Breed predisposition only. Integration of imaging and neurological findings.

When CSF flow is obstructed proximally, the most likely consequence is: Peripheral nerve dysfunction. Ventricular dilation proximal to the obstruction. Immediate skull collapse. Decreased CSF volume.

The key feature distinguishing hydrocephalus ex-vacuo is: CSF expansion secondary to brain tissue loss. Congenital skull deformity. Exclusive CSF overproduction. Primary obstruction of CSF flow.

Toy breeds are predisposed to congenital hydrocephalus primarily due to: Increased CSF absorption capacity. Peripheral nerve fragility. Reduced ventricular size. Breed predisposition to congenital hydrocephalus.

Medical therapy alone is unlikely to: Provide symptomatic improvement. Permanently correct the underlying CSF flow disturbance. Be used in mild cases. Reduce CSF production temporarily.

When ventriculomegaly is detected on MRI, the correct approach is to: Diagnose hydrocephalus immediately. Recommend surgery in all cases. Ignore clinical signs. Correlate imaging findings with clinical examination.

When deciding between medical and surgical management, clinicians should primarily assess: Breed alone. Clinical severity, progression and response to therapy. Owner preference exclusively. Ventricular size alone.

Long-term follow-up of hydrocephalus patients is important to monitor: Hair coat changes. Neurological progression and response to therapy. Body weight only. Peripheral nerve conduction.

Which surgical techniques are explicitly listed in the lecture notes under surgical management?. Foramen magnum decompression and dorsal laminectomy. Transsphenoidal hypophysectomy and craniotomy for tumour excision. Ventriculoatrial shunt placement and ventriculoperitoneal shunt placement. Hemilaminectomy and ventral slot.

According to the review, which bacterial group is most frequently isolated in shunt infections (human data, with dogs possibly analogous)?. Staphylococcus spp. Mycoplasma spp. Leptospira spp. Bordetella spp.

Hydrocephalus should be understood primarily as a disorder of: Peripheral nerve conduction. Cerebellar development only. Muscle metabolism. CSF circulation.

A ventriculoperitoneal shunt works by: Diverting CSF from ventricles to the peritoneal cavity. Closing the aqueduct. Blocking CSF production permanently. Reducing skull size.

The location of CSF obstruction determines: Breed predisposition. Presence of peripheral neuropathy. Whether hydrocephalus is communicating or noncommunicating. Skull size exclusively.

Blindness in hydrocephalus without ocular abnormalities indicates: Primary retinal degeneration. Forebrain involvement. Peripheral nerve disorder. Optic nerve trauma only.

Which option lists medications mentioned in the notes specifically under 'To treat seizures'?. Only mannitol. Acetazolamide, furosemide, and prednisone. Diazepam, potassium bromide (KBr), and phenobarbital. Only antibiotics.

Ventriculoperitoneal shunting is most appropriately indicated when: The skull is dome-shaped only. Ventricles are slightly enlarged without signs. Deficits are severe, progressive, or unresponsive to medical therapy. The dog is a toy breed.

Why is imaging alone insufficient to diagnose clinically significant hydrocephalus?. Because ventriculomegaly may occur in neurologically normal animals. Because skull shape determines diagnosis. Because MRI cannot visualize ventricles. Because seizures confirm hydrocephalus.

CSF is primarily absorbed at the level of the: Arachnoid villi within the subarachnoid space. Spinal cord grey matter. Choroid plexus. Cranial sutures.

According to the review, cerebrospinal fluid (CSF) is primarily produced in the: Subarachnoid space only. Spinal nerve roots. Choroid plexus within the ventricular system. Cerebellar cortex.

Initial management of mild clinical hydrocephalus often involves: No treatment regardless of signs. Peripheral nerve therapy. Immediate ventriculoperitoneal shunting. Medical therapy to reduce CSF production.

Surgical shunting should be considered when: Medical therapy fails or deficits are severe/progressive. Only when seizures are absent. Only in geriatric patients. All patients at diagnosis.

Hydrocephalus fundamentally results from disturbance of: Neuromuscular transmission. Peripheral nerve conduction. Cerebellar metabolism. CSF circulation from production to absorption.

According to the notes, ventriculomegaly should be interpreted as: Always associated with severe neurological deficits. Not synonymous with hydrocephalus and may be present in neurologically normal dogs. Irrelevant in diagnostic evaluation. Always diagnostic of hydrocephalus.

Failure to learn simple tasks in a young hydrocephalic dog reflects dysfunction of the: Peripheral nerve. Brainstem. Spinal cord. Forebrain.

If ventriculomegaly is present but neurological examination is normal, the clinician should: Correlate imaging with clinical findings before diagnosing hydrocephalus. Immediately recommend surgery. Ignore clinical examination. Diagnose active hydrocephalus.

Hydrocephalus develops when there is an imbalance between: CSF production and absorption. Neurotransmitter release and uptake. Peripheral nerve conduction velocities. Muscle contraction and relaxation.

Communicating hydrocephalus is characterized by: Complete blockage within the lateral ventricles. Absence of CSF production. Peripheral neuropathy signs. Persistence of communication between ventricles and subarachnoid space.

The functional goal of a ventriculoperitoneal shunt is to: Stimulate CSF overproduction. Repair brain parenchyma directly. Increase skull volume. Divert CSF to control ventricular dilation.

The prognosis of congenital hydrocephalus is described as: Uniformly fatal in neonates. Identical in all breeds. Always benign and self-limiting. Variable depending on severity and response to therapy.

Obtundation in a hydrocephalic dog indicates: Cervical disc disease. Muscle weakness only. Peripheral nerve degeneration. Altered mentation from forebrain dysfunction.

Which option best matches the treatment principles described in the review and notes for hydrocephalus?. Medical therapy aims to decrease CSF production; surgical shunting aims to establish controlled CSF flow and is recommended when medical therapy fails or deficits are severe/progressive. Surgery is recommended for all dogs at diagnosis because ventricular size always correlates with clinical severity. Medical therapy increases CSF production to improve circulation; surgery is contraindicated in congenital cases. Medical therapy aims to permanently cure hydrocephalus; surgery is only for mild, non-progressive cases.

The dome-shaped skull in toy breeds with hydrocephalus results primarily from: Primary cerebellar hypoplasia. Peripheral nerve swelling. Skull expansion due to open sutures and increased intracranial pressure. Muscle hypertrophy.

Altered mentation in hydrocephalus patients most commonly indicates dysfunction of the: Lumbar spinal cord. Forebrain. Neuromuscular junction. Peripheral nerve.

Circling behavior in hydrocephalus is most consistent with: Peripheral vestibular disease. Forebrain dysfunction. Lumbar spinal lesion. Neuromuscular junction disease.