The most common cause of failure to be able to close the mouth is a trigeminal neuropathy. The trigeminal nerve is cranial nerve V and is responsible for sensation in the face and motor functions such as biting and chewing. Here's a synopsis of this disorder for you:
Definition: An idiopathic, self-limiting inflammatory condition that involves the motor and sensory branches of the trigeminal nerve and (on occasion) the sympathetic innervation to the eye (i.e., Horner's syndrome)
Synonym: Dropped jaw
Epidemiology (Species, Age, Sex): Dogs most commonly affected; rare in cats
Genetics and Breed Predisposition
No sex or breed predilection; golden retrievers may be overrepresented.
Risk Factors: Other immune-mediated disease
Associated Disorders: Possible paraneoplastic association (related to a cancer elsewhere in the body)
Bilateral paralysis of the masticatory muscles that primarily affects the mandibular branch of the trigeminal nerve
History, Chief Complaint
Acute or subacute onset of an inability to close the mouth. The dog cannot prehend food, may hypersalivate, and has difficulty drinking water.
Physical Exam Findings
Bilateral paralysis of the masticatory muscles
Affected dogs are bright and alert and do not appear as though they are in pain. Most have no other detectable neurologic abnormalities.
In some cases, there is decreased facial sensation bilaterally, and Horner's syndrome may be observed.
Trismus/inability to open the mouth does not occur with trigeminal neuritis.
Etiology and Pathophysiology
Most common neurologic cause of an inability to close the mouth in the dog
Etiology is unknown, but extensive bilateral nonsuppurative inflammation, demyelination, and, in some cases, axonal degeneration of all portions of the trigeminal nerve and its ganglion, with no brainstem lesions, have been reported at necropsy.
Complete recovery is observed in 2-3 weeks (rarely, may take several months), with no drug therapy being reported as useful.
Facial sensation is usually preserved. Occasionally, Horner's syndrome may be observed, presumably because the postganglionic sympathetic axons course with the ophthalmic branch of the trigeminal nerve.
Diagnostic Overview: The diagnosis is based on characteristic clinical signs, absence of other neurologic deficits, and elimination of the possibility of orthopedic (mandibular, temporomandibular joint) disorders. Advanced diagnostic testing is generally reserved for cases showing additional or unusual neurologic deficits, when spontaneous resolution does not occur, or if rabies is possible (quarantine/euthanasia).
Traumatic mandibular injury
Inflammatory or infectious central nervous system (CNS) disease
CBC, serum chemistry profile, urinalysis: usually within normal limits
Screening for infectious diseases such as protozoal, fungal, and viral diseases is recommended, as clinically and geographically appropriate.
Advanced or Confirmatory Testing
Unnecessary in most cases
Cerebrospinal fluid (CSF) analysis may be normal or show mild increases in protein concentration. Lymphocytic pleocytosis is rarely observed.
Electromyography may reveal increased insertional activity and other mild changes.
Computed tomography or magnetic resonance imaging of the brain: within normal limits
trigeminal nerve biopsy: not recommended
Treatment: Spontaneous recovery usually occurs in 2-3 weeks. Please respond with further questions or concerns if you wish.